The DOI matches its Crossref record; 150 of the 151 references it cites were found in a registry or an index; 2 of the 170 sources its claims cite were checked for support.
Mitochondria Initiate and Regulate Sarcopenia
Open accessAbstract
We present the hypothesis that an accumulation of dysfunctional mitochondria initiates a signaling cascade leading to motor neuron and muscle fiber death and culminating in sarcopenia. Interactions between neural and muscle cells that contain dysfunctional mitochondria exacerbate sarcopenia. Preventing sarcopenia will require identifying mitochondrial sources of dysfunction that are reversible.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This review proposes that age-related accumulation of dysfunctional mitochondria in muscle cells and motor neurons initiates apoptotic signaling and cell death, leading to sarcopenia, with neural–muscle cross talk exacerbating the process. It argues that preventing sarcopenia requires identifying reversible mitochondrial sources of dysfunction, especially through mitophagy, exercise, and nutrition.
Key findings
- The central hypothesis is that mitochondrial deterioration in muscles and motor neurons is the primary initiator of sarcopenia; increased mPTP opening releases mitochondrial contents to the cytosol, initiating apoptosis and nuclear DNA fragmentation, leading to fiber and motor neuron death.
- Sarcopenia in aged humans and rodents is associated with motor neuronal death, impaired innervation, and a ~27% reduction in the motor unit pool; loss of innervation induces profound muscle atrophy.
- Proposed mitochondrial sources of damage include ROS, mtDNA deletions/mutations, and denervation; aging also attenuates mitophagy, allowing dysfunctional mitochondria to persist, with Mfn2 decline implicated as a possible bridge, though conflicting data exist.
- Exercise and nutritional interventions are proposed to improve mitochondrial health by increasing mitophagy and mitochondrial biogenesis, but the paper notes uncertainty about whether new mitochondria in aged hosts are healthy and whether antioxidants should be used when elderly begin exercise.
Methods
- Design: conceptual/hypothesis review; no primary experimental study is reported.
- Data or sample: Not stated in the paper; the paper cites published studies in aged humans, rodents, and cell/mouse models rather than presenting its own sample.
- Main analysis: narrative synthesis and development of hypothetical models (Figures 1 and 2); no formal statistical or systematic analysis is reported.
Limitations
- The paper states the hypothesis is based on speculation and requires additional work; it specifically notes lack of data for aging-associated localized motor neuron disassembly outside neural degenerative disease.
- The paper acknowledges conflicting evidence, including whether Mfn2 declines or mitophagy is reduced in aged muscle, and inconsistent UPS/atrogene findings across studies.
- Evident from the text: as a narrative review, it provides no primary data, systematic search, or causal test of the mitochondrial-initiation hypothesis.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
80 Not checked yet · 26 Own interpretation · 1 Partly supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“studies that have reported a higher fusion index in muscles from old rodents as indicated by ratios of Mfn1/Mfn2 (63) or Mfn2/Drp1 (75) did not find changes in the protein contents of Mfn1, Mfn2, Opa1 or Drp1.”
§ Mitochondria Initiate and Regulate Sarcopenia > Local apoptotic signaling in aging muscles and motor neurons becomes more wide spread to result in cell death > Altered mitochondrial dynamics with aging
What the sources say
- Partly supportedcites [63] Joseph AM Adhihetty PJ Wawrzyniak NR Wohlgemuth SE Picca A Kujoth GC Prolla TA Leeuwenburgh C Dysregulation of mitochondrial quality control processes contribute to sarcopenia in a mouse model of premature aging PLoS. One 2013 8 e69327 23935986 PMC3720551 sourceExperimental — accuracy not yet measured
The Results (‘Altered Mitochondrial Morphology Proteins in mtDNA Mutator Mice’) report no changes in Opa1 or Drp1, supporting that part of the claim. But Mfn1 and Mfn2 were significantly higher in older than younger mice, so the claim that their protein contents did not change is not supported. Table 1 in the Discussion confirms this distinction for normally aging mice. (LLM, conf=0.88)
- Supportedcites [75] Leduc-Gaudet JP Picard M Jean PF St Sgarioto N Auger MJ Vallee J Robitaille R Pierre DH St Gouspillou G Mitochondrial morphology is altered in atrophied skeletal muscle of aged mice Oncotarget 2015 6 17923 17937 26053100 PMC4627226 source
The Results section (Figure 6) reports a significantly increased Mfn2-to-Drp1 ratio in aged mouse skeletal muscle, while finding no significant differences in Opa1, Mfn1, Mfn2, or Drp1 protein content. This supports the part of the citing sentence attributed to this paper. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
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- Partly supported
In the paper
“both neural and muscle losses of the cytosolic antioxidant CuZn-superoxide dismutase (CuZnSOD) recapitulated sarcopenic muscle loss in a mouse model (125).”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
What the sources say
- Not checked yetcites [125] Sataranatarajan K Qaisar R Davis C Sakellariou GK Vasilaki A Zhang Y Liu Y Bhaskaran S McArdle A Jackson M Brooks SV Richardson A Van RH Neuron specific reduction in CuZnSOD is not sufficient to initiate a full sarcopenia phenotype Redox. Biol 2015 5 140 148 25917273 PMC5022075 source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“it is clear that accumulation of excessive ROS contributes to damaged and dysfunctional mitochondria in muscle and neural cells.”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
What the sources say
- Not checked yetcites [15] Brand MD Mitochondrial generation of superoxide and hydrogen peroxide as the source of mitochondrial redox signaling Free Radic. Biol. Med 2016 27085844 source
- Not checked yetcites [125] Sataranatarajan K Qaisar R Davis C Sakellariou GK Vasilaki A Zhang Y Liu Y Bhaskaran S McArdle A Jackson M Brooks SV Richardson A Van RH Neuron specific reduction in CuZnSOD is not sufficient to initiate a full sarcopenia phenotype Redox. Biol 2015 5 140 148 25917273 PMC5022075 source
boosteddirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“It is interesting that a loss of mitochondria function with aging is a mechanism that is shared by both muscle cells (18, 63) and motor neurons (123).”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction
What the sources say
- Not checked yetcites [18] Calvani R Joseph AM Adhihetty PJ Miccheli A Bossola M Leeuwenburgh C Bernabei R Marzetti E Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy Biol. Chem 2013 394 393 414 23154422 PMC3976204 source
- Not checked yetcites [63] Joseph AM Adhihetty PJ Wawrzyniak NR Wohlgemuth SE Picca A Kujoth GC Prolla TA Leeuwenburgh C Dysregulation of mitochondrial quality control processes contribute to sarcopenia in a mouse model of premature aging PLoS. One 2013 8 e69327 23935986 PMC3720551 source
- Not checked yetcites [123] Rygiel KA Grady JP Turnbull DM Respiratory chain deficiency in aged spinal motor neurons Neurobiol. Aging 2014 35 2230 2238 24684792 PMC4099519 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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In the paper
“the absence of CuZnSOD in either neural or muscle cells did not manifest full sarcopenic muscle loss (125).”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
What the sources say
- Not checked yetcites [125] Sataranatarajan K Qaisar R Davis C Sakellariou GK Vasilaki A Zhang Y Liu Y Bhaskaran S McArdle A Jackson M Brooks SV Richardson A Van RH Neuron specific reduction in CuZnSOD is not sufficient to initiate a full sarcopenia phenotype Redox. Biol 2015 5 140 148 25917273 PMC5022075 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“In aging, a loss of innervation induces profound muscle atrophy (5, 106, 129).”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction
What the sources say
- Not checked yetcites [5] Alway SE Degens H Krishnamurthy G Chaudhrai A Denervation stimulates apoptosis but not Id2 expression in hindlimb muscles of aged rats J Gerontol. A Biol. Sci Med Sci 2003 58 687 697 12902526 source
- Not checked yetcites [106] Pannerec A Springer M Migliavacca E Ireland A Piasecki M Karaz S Jacot G Metairon S Danenberg E Raymond F Descombes P McPhee JS Feige JN A robust neuromuscular system protects rat and human skeletal muscle from sarcopenia Aging (Albany. NY) 2016 8 712 729 27019136 PMC4925824
- Not checked yetcites [129] Siu PM Alway SE Mitochondria-associated apoptotic signalling in denervated rat skeletal muscle J. Physiol 2005 565 309 323 15774533 PMC1464486 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, mitochondrial susceptibility to mPTP opening is a common point which triggers downstream cell destruction in both neuron and muscle cells.”
§ Mitochondria Initiate and Regulate Sarcopenia > Mitochondria permeability transition pore sensitization with aging – mitochondrial dysfunction
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“electron microscopy and biochemical analyses have shown small, more fragmented mitochondria in muscles from old as compared to young adult hosts (56, 57)”
§ Mitochondria Initiate and Regulate Sarcopenia > Local apoptotic signaling in aging muscles and motor neurons becomes more wide spread to result in cell death > Altered mitochondrial dynamics with aging
What the sources say
- Not checked yetcites [56] Iqbal S Hood DA The role of mitochondrial fusion and fission in skeletal muscle function and dysfunction Front Biosci. (Landmark. Ed) 2015 20 157 172 25553445 source
- Not checked yetcites [57] Iqbal S Ostojic O Singh K Joseph AM Hood DA Expression of mitochondrial fission and fusion regulatory proteins in skeletal muscle during chronic use and disuse Muscle Nerve 2013 48 963 970 23494933 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Defective mitophagy underlies the progression of motor neuron death in Amyotrophic lateral sclerosis (ALS) (38).”
§ Mitochondria Initiate and Regulate Sarcopenia > Insufficient mitophagy allows unhealthy mitochondria to persist in aging muscles and neurons
What the sources say
- Not checked yetcites [38] Fornai F Longone P Ferrucci M Lenzi P Isidoro C Ruggieri S Paparelli A Autophagy and amyotrophic lateral sclerosis: The multiple roles of lithium Autophagy 2008 4 527 530 18367867 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Our model for a localized apoptotic and proteolytic signaling cascade that expands to neighboring regions of a muscle fiber (Figure 2) has strong support from the work of Aiken and co-workers (26, 49, 50).”
§ Mitochondria Initiate and Regulate Sarcopenia > Local apoptotic signaling in aging muscles and motor neurons becomes more wide spread to result in cell death
What the sources say
- Not checked yetcites [26] Cheema N Herbst A McKenzie D Aiken JM Apoptosis and necrosis mediate skeletal muscle fiber loss in age-induced mitochondrial enzymatic abnormalities Aging Cell 2015 14 1085 1093 26365892 PMC4693455 source
- Not checked yetcites [49] Herbst A Pak JW McKenzie D Bua E Bassiouni M Aiken JM Accumulation of mitochondrial DNA deletion mutations in aged muscle fibers: evidence for a causal role in muscle fiber loss J Gerontol. A Biol. Sci. Med. Sci 2007 62 235 245 17389720 PMC2846622 source
- Not checked yetcites [50] Herbst A Wanagat J Cheema N Widjaja K McKenzie D Aiken JM Latent mitochondrial DNA deletion mutations drive muscle fiber loss at old age Aging Cell 2016 PMC5114866 27561813
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Probably not a substantial claim. 12
- It may state two separate claims as one. 38
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Cross talk between muscles and motor neurons that contain dysfunctional mitochondria exacerbates sarcopenia.”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
plaindirect- Asserted: fails — The authors may not put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The authors may not put it forward as true. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A loss of mitophagy-proteasome-induced mitochondrial clearance in muscle and motor neuron cells promotes accumulation of poorly functioning mitochondria that have increased mPTP opening.”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
plaindirect- Asserted: fails — The authors may not put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The authors may not put it forward as true. The paper may give no reason why it holds.
- Rests on an assumption: Aging suppression of autophagy activators such as SIRT1 and Mfn2 prevents removal of dysfunctional mitochondria via mitophagy and proteasome digestion.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Removal of nuclei in muscle cells and motor neurons leads to fiber and motor neuron death and loss of innervation to the muscle cells.”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
- The authors state this as an assumption: Leaked mitochondrial contents initiate intrinsic apoptotic signaling leading to DNA fragmentation and nuclear apoptosis in a localized fiber region.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Aging increases mitochondrial stress that sensitizes the opening of the mitochondria transition permeability pore (mPTP).”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
plaindirect- Asserted: fails — The authors may not put it forward as true.
- Checkable: passes — It can be checked against evidence.
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- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The authors may not put it forward as true. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“sarcopenia in aged humans and rodents is also associated with motor neuronal death (96, 139), which causes impaired innervation (48, 106), and a ~27% reduction in the motor unit pool.”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction
What the sources say
- Not checked yetcites [96] Mittal KR Logmani FH Age-related reduction in 8th cervical ventral nerve root myelinated fiber diameters and numbers in man J Gerontol 1987 42 8 10 3794203
- Not checked yetcites [139] Tomlinson BE Irving D The numbers of limb motor neurons in the human lumbosacral cord throughout life J Neurol. Sci 1977 34 213 219 925710
- Not checked yetcites [48] Hepple RT Rice CL Innervation and neuromuscular control in ageing skeletal muscle J Physiol 2016 594 1965 1978 26437581 PMC4933121
- Not checked yetcites [106] Pannerec A Springer M Migliavacca E Ireland A Piasecki M Karaz S Jacot G Metairon S Danenberg E Raymond F Descombes P McPhee JS Feige JN A robust neuromuscular system protects rat and human skeletal muscle from sarcopenia Aging (Albany. NY) 2016 8 712 729 27019136 PMC4925824
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our current perspective and hypothesis is that mitochondrial deterioration in muscles and motor neurons is the primary initiator of sarcopenia (Figure 1).”
- Also stated in: § Mitochondrial regulation of sarcopenia - Hypothesis · plain
“Thus, mitochondria are key initiators and regulators of sarcopenia (Figure 1).”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
- The authors state this as an assumption: Local mitochondrial damage causes increased mPTP opening.
- The authors state this as an assumption: mPTP opening triggers mitochondrial contents to leak into the cytosol.
- The authors state this as an assumption: Leaked mitochondrial contents initiate intrinsic apoptotic signaling leading to DNA fragmentation and nuclear apoptosis in a localized fiber region.
- Rests on an assumption: Aging suppression of autophagy activators such as SIRT1 and Mfn2 prevents removal of dysfunctional mitochondria via mitophagy and proteasome digestion.
- Also stated in: § Mitochondrial regulation of sarcopenia - Hypothesis · plain
None of the sources cited for this claim have been checked yet.
In the paper
“Aging increases ROS production (22), and lowers antioxidant enzymes levels in muscle and neuron cells (58, 59, 121).”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
What the sources say
- Not checked yetcites [22] Carter HN Chen CC Hood DA Mitochondria, muscle health, and exercise with advancing age Physiology. (Bethesda.) 2015 30 208 223 25933821
- Not checked yetcites [58] Jackson JR Ryan MJ Alway SE Long-term supplementation with resveratrol alleviates oxidative stress but does not attenuate sarcopenia in aged mice J Gerontol. A Biol. Sci Med. Sci 2011 66 751 764 21454355 PMC3143346
- Not checked yetcites [59] Jackson JR Ryan MJ Hao Y Alway SE Mediation of endogenous antioxidant enzymes and apoptotic signaling by resveratrol following muscle disuse in the gastrocnemius muscles of young and old rats Am. J Physiol Regul. Integr. Comp Physiol 2010 299 R1572 R1581 20861279 PMC3007185
- Not checked yetcites [121] Ryan MJ Jackson JR Hao Y Leonard SS Alway SE Inhibition of xanthine oxidase reduces oxidative stress and improves skeletal muscle function in response to electrically stimulated isometric contractions in aged mice Free Radic. Biol. Med 2011 51 38 52 21530649 PMC3430730
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Mitochondrial DNA (mtDNA) deletions or DNA mutations contribute to mitochondrial dysfunction and aging-related muscle fiber loss and atrophy (50, 90).”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
What the sources say
- Not checked yetcites [50] Herbst A Wanagat J Cheema N Widjaja K McKenzie D Aiken JM Latent mitochondrial DNA deletion mutations drive muscle fiber loss at old age Aging Cell 2016 PMC5114866 27561813
- Not checked yetcites [90] McKenzie D Bua E McKiernan S Cao Z Aiken JM Mitochondrial DNA deletion mutations: a causal role in sarcopenia Eur. J Biochem 2002 269 2010 2015 11985577
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Leakage of the mitochondrial contents to the cell cytosol initiates death (apoptosis) signaling in muscle cells and motor neurons, which contributes to nuclear DNA fragmentation and if not repaired, nuclear apoptosis.”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
plaindirect- Asserted: fails — The authors may not put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The authors may not put it forward as true. The paper may give no reason why it holds. It may state two separate claims as one.
- The authors state this as an assumption: mPTP opening triggers mitochondrial contents to leak into the cytosol.
- The authors state this as an assumption: Leaked mitochondrial contents initiate intrinsic apoptotic signaling leading to DNA fragmentation and nuclear apoptosis in a localized fiber region.
None of the sources cited for this claim have been checked yet.
In the paper
“Sarcopenia, is associated with increased levels of apoptosis (47) and reduced capabilities for muscle regeneration (41) leading to muscle wasting.”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction
What the sources say
- Not checked yetcites [47] Hao Y Jackson JR Wang Y Edens N Pereira SL Alway SE ß-Hydroxy-ß-methylbutyrate reduces myonuclear apoptosis during recovery from hind limb suspension-induced muscle fiber atrophy in aged rats Am. J. Physiol Regul. Integr. Comp Physiol 2011 301 R701 R715 21697520 PMC3174754
- Not checked yetcites [41] Garcia-Prat L Sousa-Victor P Munoz-Canoves P Functional dysregulation of stem cells during aging: a focus on skeletal muscle stem cells FEBS J 2013 280 4051 4062 23452120 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Some denervated fibers become innervated by axons from surviving motor neurons (42, 45), whereas other fibers remain denervated and contribute to functional losses in sarcopenia (42).”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction
What the sources say
- Not checked yetcites [42] Gilmore KJ Morat T Doherty TJ Rice CL Motor Unit Number Estimations and Neuromuscular Fidelity in Three Stages of Sarcopenia Muscle Nerve 2016 27576772
- Not checked yetcites [45] Gutmann E Hanzlikova V Denervation, reinnervation and regeneration of senile muscle Adv. Exp. Med Biol 1975 53 431 440 123404
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Opening the mPTP induces a further loss of mitochondrial membrane potential, and releases the mitochondrial contents to the cytosol to initiate apoptotic signaling (24, 77, 89).”
§ Mitochondria Initiate and Regulate Sarcopenia > Mitochondria permeability transition pore sensitization with aging – mitochondrial dysfunction
What the sources say
- Not checked yetcites [24] Chabi B Ljubicic V Menzies KJ Huang JH Saleem A Hood DA Mitochondrial function and apoptotic susceptibility in aging skeletal muscle Aging. Cell 2008 7 2 12 18028258 source
- Not checked yetcites [77] Leeuwenburgh C Gurley CM Strotman BA Dupont-Versteegden EE Age-related differences in apoptosis with disuse atrophy in soleus muscle Am. J Physiol Regul. Integr. Comp Physiol 2005 288 R1288 R1296 15650125
- Not checked yetcites [89] Marzetti E Wohlgemuth SE Lees HA Chung HY Giovannini S Leeuwenburgh C Age-related activation of mitochondrial caspase-independent apoptotic signaling in rat gastrocnemius muscle Mech. Ageing. Dev 2008 129 542 549 18579179 PMC2585824 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“a knockout of Mfn 1/2 in skeletal muscle, which prevented mitochondrial fusion, increased the accumulation of mtDNA defects and resulted in muscle atrophy (31).”
§ Mitochondria Initiate and Regulate Sarcopenia > Local apoptotic signaling in aging muscles and motor neurons becomes more wide spread to result in cell death > Altered mitochondrial dynamics with aging
What the sources say
- Not checked yetcites [31] Correia-Melo C Marques FD Anderson R Hewitt G Hewitt R Cole J Carroll BM Miwa S Birch J Merz A Rushton MD Charles M Jurk D Tait SW Czapiewski R Greaves L Nelson G Bohlooly Y Rodriguez-Cuenca S Vidal-Puig A Mann D Saretzki G Quarato G Green DR Adams PD von ZT Korolchuk VI Passos JF Mitochondria are required for pro-ageing features of the senescent phenotype EMBO J 2016 35 724 742 26848154 PMC4818766 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Recent data by Sebastián and colleagues (127) show that Mfn2 declines in muscle with aging and loss of Mfn2 produces an aging-like phenotype, including age-associated mitochondrial dysfunction, higher ROS accumulation and muscle fiber atrophy.”
§ Mitochondria Initiate and Regulate Sarcopenia > Insufficient mitophagy allows unhealthy mitochondria to persist in aging muscles and neurons
What the sources say
- Not checked yetcites [127] Sebastian D Sorianello E Segales J Irazoki A Ruiz-Bonilla V Sala D Planet E Berenguer-Llergo A Munoz JP Sanchez-Feutrie M Plana N Hernandez-Alvarez MI Serrano AL Palacin M Zorzano A Mfn2 deficiency links age-related sarcopenia and impaired autophagy to activation of an adaptive mitophagy pathway EMBO J 2016 35 1677 1693 27334614 PMC4969577 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“other studies have found higher fusion profiles in muscles of humans (14), and prematurely aged mice (63), and larger mitochondria in muscles of old mice (75).”
§ Mitochondria Initiate and Regulate Sarcopenia > Local apoptotic signaling in aging muscles and motor neurons becomes more wide spread to result in cell death > Altered mitochondrial dynamics with aging
What the sources say
- Not checked yetcites [14] Bori Z Zhao Z Koltai E Fatouros IG Jamurtas AZ Douroudos II Terzis G Chatzinikolaou A Sovatzidis A Draganidis D Boldogh I Radak Z The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle Exp. Gerontol 2012 47 417 424 22449457 PMC4915826
- Not checked yetcites [63] Joseph AM Adhihetty PJ Wawrzyniak NR Wohlgemuth SE Picca A Kujoth GC Prolla TA Leeuwenburgh C Dysregulation of mitochondrial quality control processes contribute to sarcopenia in a mouse model of premature aging PLoS. One 2013 8 e69327 23935986 PMC3720551 source
- Not checked yetcites [75] Leduc-Gaudet JP Picard M Jean PF St Sgarioto N Auger MJ Vallee J Robitaille R Pierre DH St Gouspillou G Mitochondrial morphology is altered in atrophied skeletal muscle of aged mice Oncotarget 2015 6 17923 17937 26053100 PMC4627226 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
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In the paper
“aging-induced mtDNA deletions are closely associated with a loss of mitochondrial function in motor neurons (123), neuronal malfunction in diseases like Parkinson’s disease (115), and muscle loss with aging (50, 91).”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
What the sources say
- Not checked yetcites [123] Rygiel KA Grady JP Turnbull DM Respiratory chain deficiency in aged spinal motor neurons Neurobiol. Aging 2014 35 2230 2238 24684792 PMC4099519
- Not checked yetcites [115] Reeve A Meagher M Lax N Simcox E Hepplewhite P Jaros E Turnbull D The impact of pathogenic mitochondrial DNA mutations on substantia nigra neurons J Neurosci 2013 33 10790 10801 23804100 PMC6618501
- Not checked yetcites [50] Herbst A Wanagat J Cheema N Widjaja K McKenzie D Aiken JM Latent mitochondrial DNA deletion mutations drive muscle fiber loss at old age Aging Cell 2016 PMC5114866 27561813
- Not checked yetcites [91] McKiernan SH Colman R Lopez M Beasley TM Weindruch R Aiken JM Longitudinal analysis of early stage sarcopenia in aging rhesus monkeys Exp. Gerontol 2009 44 170 176 18983905 PMC2693938
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
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In the paper
“In neurons, DNA damage precedes neuronal apoptosis (85), whereas forced repair of DNA damage rescues neurons from elimination by apoptosis (86).”
§ Mitochondria Initiate and Regulate Sarcopenia > Introduction > Mitochondrial regulation of sarcopenia - Hypothesis
What the sources say
- Not checked yetcites [85] Martin LJ Liu Z Injury-induced spinal motor neuron apoptosis is preceded by DNA single-strand breaks and is p53- and Bax-dependent J Neurobiol 2002 50 181 197 11810634
- Not checked yetcites [86] Martin LJ Wong M Enforced DNA repair enzymes rescue neurons from apoptosis induced by target deprivation and axotomy in mouse models of neurodegeneration Mech. Ageing Dev 2016 PMC5192008 27364693
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“muscles of aged rodents and humans have a greater overall rate of fission vs. fusion (55, 62) and lower levels of the fusion protein Opa1 (62) as compared with younger muscles.”
§ Mitochondria Initiate and Regulate Sarcopenia > Local apoptotic signaling in aging muscles and motor neurons becomes more wide spread to result in cell death > Altered mitochondrial dynamics with aging
What the sources say
- Not checked yetcites [55] Ibebunjo C Chick JM Kendall T Eash JK Li C Zhang Y Vickers C Wu Z Clarke BA Shi J Cruz J Fournier B Brachat S Gutzwiller S Ma Q Markovits J Broome M Steinkrauss M Skuba E Galarneau JR Gygi SP Glass DJ Genomic and proteomic profiling reveals reduced mitochondrial function and disruption of the neuromuscular junction driving rat sarcopenia Mol. Cell Biol 2013 33 194 212 23109432 PMC3554128
- Not checked yetcites [62] Joseph AM Adhihetty PJ Buford TW Wohlgemuth SE Lees HA Nguyen LM Aranda JM Sandesara BD Pahor M Manini TM Marzetti E Leeuwenburgh C The impact of aging on mitochondrial function and biogenesis pathways in skeletal muscle of sedentary high- and low-functioning elderly individuals Aging Cell 2012 11 801 809 22681576 PMC3444680 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“fiber atrophy and apoptotic signaling did not occur in other regions of the same muscle fibers that were located further away from the dysfunctional mitochondrial (26).”
§ Mitochondria Initiate and Regulate Sarcopenia > Local apoptotic signaling in aging muscles and motor neurons becomes more wide spread to result in cell death
What the sources say
- Not checked yetcites [26] Cheema N Herbst A McKenzie D Aiken JM Apoptosis and necrosis mediate skeletal muscle fiber loss in age-induced mitochondrial enzymatic abnormalities Aging Cell 2015 14 1085 1093 26365892 PMC4693455
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“If the degenerative processes were not initiated locally but rather from a more general or systemic source, we would expect uniform muscle fiber wasting across its length, but this is not the case.”
§ Mitochondria Initiate and Regulate Sarcopenia > Local apoptotic signaling in aging muscles and motor neurons becomes more wide spread to result in cell death
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“Cheema et al. (26) observed a localized aging-induced loss of the mitochondrial enzymes succinate dehydrogenase and cytochrome c oxidase. Interestingly, the same fiber region that had mitochondrial disruption was both atrophic and had high levels of the apoptotic protein caspase-3.”
§ Mitochondria Initiate and Regulate Sarcopenia > Local apoptotic signaling in aging muscles and motor neurons becomes more wide spread to result in cell death
What the sources say
- Not checked yetcites [26] Cheema N Herbst A McKenzie D Aiken JM Apoptosis and necrosis mediate skeletal muscle fiber loss in age-induced mitochondrial enzymatic abnormalities Aging Cell 2015 14 1085 1093 26365892 PMC4693455
plaincorrelational- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“An acceleration of protein turnover with a net loss of protein is downstream of dysfunctional mitochondria but this represents a major contributor to sarcopenia.”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“FOXOs control the mammalian target of rapamycin complex 1 (MTORC1) signaling, which is associated with muscle hypertrophy (43) and inhibition of mitophagy in skeletal muscle (23).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia
What the sources say
- Not checked yetcites [43] Goodman CA Frey JW Mabrey DM Jacobs BL Lincoln HC You JS Hornberger TA The role of skeletal muscle mTOR in the regulation of mechanical load-induced growth J Physiol 2011 589 5485 5501 21946849 PMC3240886
- Not checked yetcites [23] Castets P Ruegg MA MTORC1 determines autophagy through ULK1 regulation in skeletal muscle Autophagy 2013 9 1435 1437 23896646
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“when toxins or other compounds are injected into muscles, the compounds undergo retrograde transport to the neuromuscular junction (105), deposit in motor neurons (11), and sometimes contributes to motor neuronal dysfunction (reviewed in (33, 39).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > Communication between mitochondrial induced death signaling in muscle and motor neuron cells accelerate cell death in aging
What the sources say
- Not checked yetcites [105] Pamphlett R Bayliss A Lead uptake in motor axons Muscle Nerve 1992 15 620 625 1584254
- Not checked yetcites [11] Arvidson B Inorganic mercury is transported from muscular nerve terminals to spinal and brainstem motoneurons Muscle Nerve 1992 15 1089 1094 1383815
- Not checked yetcites [33] Deinhardt K Schiavo G Endocytosis and retrograde axonal traffic in motor neurons Biochem. Soc. Symp 2005 139 150 15649138
- Not checked yetcites [39] Garcia ML Fernandez A Solas MT Mitochondria, motor neurons and aging J Neurol. Sci 2013 330 18 26 23628465
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“spinal cord injury or denervation induces large-scale muscle wasting (57, 76, 107, 129, 131, 137), and denervation is a condition often seen as part of sarcopenia.”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > Communication between mitochondrial induced death signaling in muscle and motor neuron cells accelerate cell death in aging
What the sources say
- Not checked yetcites [57] Iqbal S Ostojic O Singh K Joseph AM Hood DA Expression of mitochondrial fission and fusion regulatory proteins in skeletal muscle during chronic use and disuse Muscle Nerve 2013 48 963 970 23494933 source
- Not checked yetcites [76] Lee G Lim JY Frontera WR Apoptosis in young and old denervated rat skeletal muscle Muscle Nerve 2016 27312511
- Not checked yetcites [107] Pelletier CA Miyatani M Giangregorio L Craven BC Sarcopenic Obesity in Adults With Spinal Cord Injury: A Cross-Sectional Study Arch. Phys. Med Rehabil 2016 97 1931 1937 27282328
- Not checked yetcites [129] Siu PM Alway SE Mitochondria-associated apoptotic signalling in denervated rat skeletal muscle J. Physiol 2005 565 309 323 15774533 PMC1464486
- Not checked yetcites [131] Siu PM Alway SE Deficiency of the Bax gene attenuates denervation-induced apoptosis Apoptosis 2006 11 967 981 16763784 PMC4317263
- Not checked yetcites [137] Thakore NP Samantaray S Park S Nozaki K Smith JA Cox A Krause J Banik NL Molecular Changes in Sub-lesional Muscle Following Acute Phase of Spinal Cord Injury Neurochem. Res 2016 41 44 52 26290268 PMC9727651
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“PGC-1α2, PGC-1α3, and PGC-1α4, have been shown to stimulate protein synthesis and attenuate UPS activity in cultured myotubes and mouse skeletal muscle (87, 119).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > UPS disruption increases dysfunctional mitochondria in muscle and neural cells
What the sources say
- Not checked yetcites [87] Martinez-Redondo V Jannig PR Correia JC Ferreira DM Cervenka I Lindvall JM Sinha I Izadi M Pettersson-Klein AT Agudelo LZ Gimenez-Cassina A Brum PC Dahlman-Wright K Ruas JL Peroxisome Proliferator-activated Receptor gamma Coactivator-1 alpha Isoforms Selectively Regulate Multiple Splicing Events on Target Genes J Biol. Chem 2016 291 15169 15184 27231350 PMC4946932
- Not checked yetcites [119] Ruas JL White JP Rao RR Kleiner S Brannan KT Harrison BC Greene NP Wu J Estall JL Irving BA Lanza IR Rasbach KA Okutsu M Nair KS Yan Z Leinwand LA Spiegelman BM A PGC-1alpha isoform induced by resistance training regulates skeletal muscle hypertrophy Cell 2012 151 1319 1331 23217713 PMC3520615 source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Activated SIRT1 deacetylates and activates PCG-1α which promotes mitochondria synthesis, assembly, growth and mitochondrial antioxidant production (54).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > Cross talk between mitochondrial regulators of autophagy and the UPS
What the sources say
- Not checked yetcites [54] Hsu CP Odewale I Alcendor RR Sadoshima J Sirt1 protects the heart from aging and stress Biol. Chem 2008 389 221 231 18208353
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Inhibition of MTORC1 in muscles of tuberous sclerosis complex (TSC) knockout mice, mimic many features of aging. This includes a loss of muscle mass and strength and attenuated mitophagy (23).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia
What the sources say
- Not checked yetcites [23] Castets P Ruegg MA MTORC1 determines autophagy through ULK1 regulation in skeletal muscle Autophagy 2013 9 1435 1437 23896646
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“MuRF-1 and MAFbx expression were reported to be lower in muscles of old rats than young adult rats (35) and not changed with aging in vastus lateralis of humans (145).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia
What the sources say
- Not checked yetcites [35] Edstrom E Altun M Hagglund M Ulfhake B Atrogin-1/MAFbx and MuRF1 are downregulated in aging-related loss of skeletal muscle J Gerontol. A Biol. Sci Med Sci 2006 61 663 674 16870627
- Not checked yetcites [145] Whitman SA Wacker MJ Richmond SR Godard MP Contributions of the ubiquitin-proteasome pathway and apoptosis to human skeletal muscle wasting with age Pflugers Arch 2005 450 437 446 15952031
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“ubiquitin (17), 26S proteasome, poly-ubiquitinated proteins (3), MuRF-1 and MAFbx expression were all reported to be elevated in hindlimb muscles of sarcopenic rats as compared to young adult animals (3, 30).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia
What the sources say
- Not checked yetcites [17] Cai D Lee KK Li M Tang MK Chan KM Ubiquitin expression is up-regulated in human and rat skeletal muscles during aging Arch. Biochem. Biophys 2004 425 42 50 15081892
- Not checked yetcites [3] Altun M Besche HC Overkleeft HS Piccirillo R Edelmann MJ Kessler BM Goldberg AL Ulfhake B Muscle wasting in aged, sarcopenic rats is associated with enhanced activity of the ubiquitin proteasome pathway J Biol. Chem 2010 285 39597 39608 20940294 PMC3000941 source
- Not checked yetcites [30] Clavel S Coldefy AS Kurkdjian E Salles J Margaritis I Derijard B Atrophy-related ubiquitin ligases, atrogin-1 and MuRF1 are up-regulated in aged rat Tibialis Anterior muscle Mech. Ageing Dev 2006 127 794 801 16949134
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“AMPK activation (118) and the Forkhead box class O (FOXO) transcription factor family regulates the ubiquitin proteasome system (UPS), and the autophagy-lysosome system.”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia
What the sources say
- Not checked yetcites [118] Romanello V Guadagnin E Gomes L Roder I Sandri C Petersen Y Milan G Masiero E Del PP Foretz M Scorrano L Rudolf R Sandri M Mitochondrial fission and remodelling contributes to muscle atrophy EMBO J 2010 29 1774 1785 20400940 PMC2876965 source
- Not checked yetcites [72] Koga H Kaushik S Cuervo AM Protein homeostasis and aging: The importance of exquisite quality control Ageing Res. Rev 2011 10 205 215 20152936 PMC2888802
- Not checked yetcites [74] Lecker SH Jagoe RT Gilbert A Gomes M Baracos V Bailey J Price SR Mitch WE Goldberg AL Multiple types of skeletal muscle atrophy involve a common program of changes in gene expression FASEB J 2004 18 39 51 14718385
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“High levels of apoptotic signaling (1, 129) and altered autophagy signaling (102, 103) with elevated UPS activity (137) occurs in muscles after spinal cord injury or denervation.”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > Communication between mitochondrial induced death signaling in muscle and motor neuron cells accelerate cell death in aging
What the sources say
- Not checked yetcites [1] Adhihetty PJ O'Leary MF Chabi B Wicks KL Hood DA Effect of denervation on mitochondrially mediated apoptosis in skeletal muscle J. Appl. Physiol 2007 102 1143 1151 17122379 source
- Not checked yetcites [129] Siu PM Alway SE Mitochondria-associated apoptotic signalling in denervated rat skeletal muscle J. Physiol 2005 565 309 323 15774533 PMC1464486
- Not checked yetcites [102] O'Leary MF Vainshtein A Carter HN Zhang Y Hood DA Denervation-induced mitochondrial dysfunction and autophagy in skeletal muscle of apoptosis-deficient animals Am. J Physiol Cell Physiol 2012 303 C447 C454 22673615
- Not checked yetcites [103] O'Leary MF Vainshtein A Iqbal S Ostojic O Hood DA Adaptive plasticity of autophagic proteins to denervation in aging skeletal muscle Am. J Physiol Cell Physiol 2013 304 C422 C430 23220115 source
- Not checked yetcites [137] Thakore NP Samantaray S Park S Nozaki K Smith JA Cox A Krause J Banik NL Molecular Changes in Sub-lesional Muscle Following Acute Phase of Spinal Cord Injury Neurochem. Res 2016 41 44 52 26290268 PMC9727651
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Deacetylation of FOXO1 and FOXO3a by SIRT1 (19, 20) mediates autophagic signaling in muscle cells, and aging attenuates SIRT1, which reduces autophagy (134).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > Cross talk between mitochondrial regulators of autophagy and the UPS
What the sources say
- Not checked yetcites [19] Canto C Gerhart-Hines Z Feige JN Lagouge M Noriega L Milne JC Elliott PJ Puigserver P Auwerx J AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity Nature 2009 458 1056 1060 19262508 PMC3616311 source
- Not checked yetcites [20] Canto C Jiang LQ Deshmukh AS Mataki C Coste A Lagouge M Zierath JR Auwerx J Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle Cell Metab 2010 11 213 219 20197054 PMC3616265 source
- Not checked yetcites [134] Tang AH Rando TA Induction of autophagy supports the bioenergetic demands of quiescent muscle stem cell activation EMBO J 2014 33 2782 2797 25316028 PMC4282556
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“High ROS can damage more mitochondria in muscle and neurons (81) and potentially elevate ROS levels even higher.”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > UPS disruption increases dysfunctional mitochondria in muscle and neural cells
What the sources say
- Not checked yetcites [81] Maharjan S Oku M Tsuda M Hoseki J Sakai Y Mitochondrial impairment triggers cytosolic oxidative stress and cell death following proteasome inhibition Sci. Rep 2014 4 5896 25077633 PMC4116626
plainconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The discrepancy between these studies might be due to variability introduced by a low number of subjects or animals in each study, and perhaps by some differences in the age and sex of the subjects that were studied.”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“motor neuron dysfunction and death may converge upon mitochondria, and mitochondrial dynamics may play an important role in regulation of neuronal function that contributes to accelerated sarcopenia.”
§ Mitochondria Initiate and Regulate Sarcopenia > Local apoptotic signaling in aging muscles and motor neurons becomes more wide spread to result in cell death > Altered mitochondrial dynamics with aging
What the sources say
- Not checked yetcites [61] Jiang Z Wang W Perry G Zhu X Wang X Mitochondrial dynamic abnormalities in amyotrophic lateral sclerosis Transl. Neurodegener 2015 4 14 26225210 PMC4518588
- Not checked yetcites [143] Wang W Zhang F Li L Tang F Siedlak SL Fujioka H Liu Y Su B Pi Y Wang X MFN2 couples glutamate excitotoxicity and mitochondrial dysfunction in motor neurons J Biol. Chem 2015 290 168 182 25416777 PMC4281719
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“PARK7 is an antioxidant protein that limits mitochondrial damage in response to oxidative stress (12) and it regulates skeletal muscle contractile protein synthesis and hypertrophy (149).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > How might exercise target dysfunctional mitochondria by mitophagy?
What the sources say
- Not checked yetcites [12] Billia F Hauck L Grothe D Konecny F Rao V Kim RH Mak TW Parkinson-susceptibility gene DJ-1/PARK7 protects the murine heart from oxidative damage in vivo Proc. Natl. Acad. Sci U. S. A 2013 110 6085 6090 23530187 PMC3625258
- Not checked yetcites [149] Yu H Waddell JN Kuang S Bidwell CA Park7 expression influences myotube size and myosin expression in muscle PLoS. One 2014 9 e92030 24637782 PMC3956870
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“We know that exercise downregulates apoptosis and upregulates mitophagy (4, 52, 128, 146).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > The potential role for mitochondrial biogenesis to reduce sarcopenia
What the sources say
- Not checked yetcites [4] Alway SE Bennett BT Wilson JC Sperringer J Mohamed JS Edens NK Pereira SL Green tea extract attenuates muscle loss and improves muscle function during disuse, but fails to improve muscle recovery following unloading in aged rats J. App. Physiol 2015 118 319 330 PMC4312851 25414242
- Not checked yetcites [52] Hood DA Mechanisms of exercise-induced mitochondrial biogenesis in skeletal muscle Appl Physiol Nutr Metab 2009 34 465 472 19448716
- Not checked yetcites [128] Sin TK Yu AP Yung BY Yip SP Chan LW Wong CS Rudd JA Siu PM Effects of long-term resveratrol-induced SIRT1 activation on insulin and apoptotic signalling in aged skeletal muscle Acta Diabetol 2015 52 1063 1075 25959421
- Not checked yetcites [146] Wohlgemuth SE Seo AY Marzetti E Lees HA Leeuwenburgh C Skeletal muscle autophagy and apoptosis during aging: effects of calorie restriction and life-long exercise Exp. Gerontol 2010 45 138 148 19903516 PMC2829942 source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“If the same processes occur in humans as is the case in rodents and non-human mammals (64), exercise, or nutritional intervention such as caloric restriction would also be expected to increase mitophagy removal of dysfunctional mitochondrial, so the mitochondria that remain are proportionally healthier (64).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > How might exercise target dysfunctional mitochondria by mitophagy?
What the sources say
- Not checked yetcites [64] Joseph AM Malamo AG Silvestre J Wawrzyniak N Carey-Love S Nguyen LM Dutta D Xu J Leeuwenburgh C Adhihetty PJ Short-term caloric restriction, resveratrol, or combined treatment regimens initiated in late-life alter mitochondrial protein expression profiles in a fiber-type specific manner in aged animals Exp. Gerontol 2013 48 858 868 23747682 PMC4550205
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Aging causes degradation and availability of LAMP2A in the lysosomal membranes (69), which reduces the effectiveness of CMA.”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > How might exercise target dysfunctional mitochondria by mitophagy?
What the sources say
- Not checked yetcites [69] Kiffin R Kaushik S Zeng M Bandyopadhyay U Zhang C Massey AC Martinez-Vicente M Cuervo AM Altered dynamics of the lysosomal receptor for chaperone-mediated autophagy with age J Cell Sci 2007 120 782 791 17284523
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“satellite cells are affected adversely by aging, mitochondrial damage and death signaling (4, 6, 7, 144)”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > The potential role for mitochondrial biogenesis to reduce sarcopenia
What the sources say
- Not checked yetcites [4] Alway SE Bennett BT Wilson JC Sperringer J Mohamed JS Edens NK Pereira SL Green tea extract attenuates muscle loss and improves muscle function during disuse, but fails to improve muscle recovery following unloading in aged rats J. App. Physiol 2015 118 319 330 PMC4312851 25414242
- Not checked yetcites [6] Alway SE Myers MJ Mohamed JS Regulation of satellite cell function in sarcopenia Frontiers of Aging Neuroscience 2014 6 1 15 PMC4170136 25295003
- Not checked yetcites [7] Alway SE Pereira SL Edens NK Hao Y Bennett BT β−Hydroxy-β-methylbutyrate (HMB) enhances the proliferation of satellite cells in fast muscles of aged rats during recovery from disuse atrophy Exp. Gerontol 2013 48 973 984 23832076
- Not checked yetcites [144] Wang X Pickrell AM Rossi SG Pinto M Dillon LM Hida A Rotundo RL Moraes CT Transient systemic mtDNA damage leads to muscle wasting by reducing the satellite cell pool Hum. Mol. Genet 2013 22 3976 3986 23760083 PMC3766186
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Both endurance and resistance exercise have been associated with elevated mitochondrial biogenesis (93, 109).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > The potential role for mitochondrial biogenesis to reduce sarcopenia
What the sources say
- Not checked yetcites [93] Menzies KJ Singh K Saleem A Hood DA Sirtuin 1-mediated effects of exercise and resveratrol on mitochondrial biogenesis J Biol. Chem 2013 288 6968 6979 23329826 PMC3591607
- Not checked yetcites [109] Porter C Reidy PT Bhattarai N Sidossis LS Rasmussen BB Resistance Exercise Training Alters Mitochondrial Function in Human Skeletal Muscle Med Sci Sports Exerc 2015 47 1922 1931 25539479 PMC4478283 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“it has been proposed that autophagy signals are necessary to achieve aerobic improvements in skeletal muscle (78).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > How might exercise target dysfunctional mitochondria by mitophagy?
What the sources say
- Not checked yetcites [78] Lira VA Okutsu M Zhang M Greene NP Laker RC Breen DS Hoehn KL Yan Z Autophagy is required for exercise training-induced skeletal muscle adaptation and improvement of physical performance FASEB J 2013 27 4184 4193 23825228 PMC4046188 source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
In the paper
“Exercise-induced Pink1 activation of Drp1 (112) could also target dysfunctional mitochondria for mitophagy.”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > How might exercise target dysfunctional mitochondria by mitophagy?
What the sources say
- Not checked yetcites [112] Pryde KR Smith HL Chau KY Schapira AH PINK1 disables the anti-fission machinery to segregate damaged mitochondria for mitophagy J Cell Biol 2016 213 163 171 27091447 PMC5084273 source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Overexpression of PARK7 reduces mitochondrial dysfunction under oxidative stress (142) which shows a direct link between autophagy and mitochondrial function.”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > How might exercise target dysfunctional mitochondria by mitophagy?
What the sources say
- Not checked yetcites [142] Wang B Cai Z Tao K Zeng W Lu F Yang R Feng D Gao G Yang Q Essential control of mitochondrial morphology and function by chaperone-mediated autophagy through degradation of PARK7 Autophagy 2016 1 14 27171370 PMC4968227
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“we would expect that altered neuronal signaling is due at least in part to high ROS production and mitochondrial dysfunction in the muscle cells, and conversely, that neural dysfunction will be communicated to muscle cells (57, 100).”
§ Mitochondria Initiate and Regulate Sarcopenia > FOXO proteins and the ubiquitin proteasome system (UPS) in muscle atrophy and sarcopenia > Communication between mitochondrial induced death signaling in muscle and motor neuron cells accelerate cell death in aging
What the sources say
- Not checked yetcites [57] Iqbal S Ostojic O Singh K Joseph AM Hood DA Expression of mitochondrial fission and fusion regulatory proteins in skeletal muscle during chronic use and disuse Muscle Nerve 2013 48 963 970 23494933 source
- Not checked yetcites [100] Muller FL Song W Jang YC Liu Y Sabia M Richardson A Van Remmen H Denervation-induced skeletal muscle atrophy is associated with increased mitochondrial ROS production Am. J. Physiol. Regul. Integr. Comp. Physiol 2007 293 R1159 R1168 17584954
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Proteasome activation leads to removal of cellular contents close to the site of dysfunctional mitochondria”
§ Mitochondria Initiate and Regulate Sarcopenia > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
The authors state this as an assumption.
Local mitochondrial damage causes increased mPTP opening.
“This model assumes that local mitochondrial damage (potentially via ROS, high calcium loads, mtDNA damage etc.) causes increased mPTP opening”
The authors state this as an assumption.
mPTP opening triggers mitochondrial contents to leak into the cytosol.
“which triggers the contents of the mitochondria to leak to the cytosol.”
The authors state this as an assumption.
Leaked mitochondrial contents initiate intrinsic apoptotic signaling leading to DNA fragmentation and nuclear apoptosis in a localized fiber region.
“This initiates the intrinsic apoptotic signaling pathway leading to DNA fragmentation and nuclear apoptosis in a localized region of the fiber.”
The paper relies on this without support.
Aging suppression of autophagy activators such as SIRT1 and Mfn2 prevents removal of dysfunctional mitochondria via mitophagy and proteasome digestion.
“An aging-suppression of autophagy activators like Sirtuin 1 (SIRT1) and Mfn2 or other proteins involved in mitophagy, prevents removal of dysfunctional mitochondria via mitophagy and proteasome digestion.”
The paper relies on this without support.
Fragmented mitochondria have lower respiratory capacity and greater ROS production, increasing susceptibility to release contents and activate the intrinsic caspase apoptotic pathway.
“Fragmented mitochondria tend to have a lower respiratory capacity, and a greater production of ROS, which increases the susceptibility of mitochondria to release its contents and activate the intrinsic caspase apoptotic pathway.”
The paper relies on this without support.
Aging is associated with high cellular ROS levels, and ROS accumulation induces mPTP opening.
“aging is associated with high cell levels of ROS and ROS accumulation is an inductor for mPTP opening.”
The paper relies on this without support.
Aging leads to systemic mitochondrial dysfunction throughout the body, possibly caused by high ROS or mtDNA damage accumulation.
“Although aging induces wide spread systemic mitochondrial dysfunction, perhaps as a result of high ROS or accumulation of mtDNA damage”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“mitochondrial dysfunction (14) are the crucial factors accountable for this pathology.”
From From mitochondria to sarcopenia: role of 17β-estradiol and testosterone (2023) · cites this paper as [14]
In the citing paper
“Figure 1 shows the general pathways initiated by mitochondrial alteration resulting in motor neuron and muscle cell death and culminating in sarcopenia (14).”
From From mitochondria to sarcopenia: role of 17β-estradiol and testosterone (2023) · cites this paper as [14]
In the citing paper
“mitophagy, as a kind of selective autophagy, can identify and degrade damaged and dysfunctional mitochondria, thus generating a self-protective coping mechanism against mitochondrial dysfunction [47]”
From Lifelong Aerobic Exercise Alleviates Sarcopenia by Activating Autophagy and Inhibiting Protein Degradation via the AMPK/PGC-1α Signaling Pathway (2021) · cites this paper as [47]
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BackgroundPINK1-Phosphorylated Mitofusin 2 Is a Parkin Receptor for Culling Damaged Mitochondria
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“Mitofusin 2 (Mfn2) has an important role regulating mitochondrial fusion, but it also acts as a receptor for Pink1 and Parkin-targeted mitophagy (27).”
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“Copyright © 2017 by the American College of Sports Medicin potential to damage cellular mitochondria (reviewed in (15)).”
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BackgroundInfluentialSlowing ageing by design: the rise of NAD+ and sirtuin-activating compounds
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“SIRT1 is important for deacetylation of mitochondrial-interacting targets like PGC-1α, FOXO3, p53, and NF-kB (reviewed in (13,110) and has been implicated in improving function and life span in aging (95).”
BackgroundMitochondria are required for pro-ageing features of the senescent phenotype
Correia‐Melo, C., Marques, F. D., Anderson, R., Hewitt, G., Hewitt, R., Cole, J., Carroll, B. M., Miwa, S., Birch, J., Merz, A., et al. (2016) · The EMBO Journal · doi:10.15252/embj.201592862 · Cited by 796 · cited 2×
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BackgroundSIRT5 Regulates the Mitochondrial Lysine Succinylome and Metabolic Networks
Rardin, M. J., He, W., Nishida, Y., Newman, J. C., Carrico, C., Danielson, S. R., Guo, A., Gut, P., Sahu, A. K., Li, B., et al. (2013) · Cell Metabolism · doi:10.1016/j.cmet.2013.11.013 · Cited by 711 · cited 1×
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Background
Research works printed but not linked: 1
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Cited by
Sorted by citations
Sarcopenia, frailty and their prevention by exercise
Nascimento, C. M., Ingles, M., Salvador-Pascual, A., Cominetti, M. R., Gomez-Cabrera, M. C., & Viña, J. (2019) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.08.035 · Cited by 396
Mitochondrial dysfunction: roles in skeletal muscle atrophy
Chen, X., Ji, Y., Liu, R., Zhu, X., Wang, K., Yang, X., Liu, B., Gao, Z., Huang, Y. H., Shen, Y., et al. (2023) · Journal of Translational Medicine · doi:10.1186/s12967-023-04369-z · Cited by 362
Post-COVID-19 acute sarcopenia: physiopathology and management
Piotrowicz, K., Gąsowski, J., Michel, J., & Veronese, N. (2021) · Aging Clinical and Experimental Research · doi:10.1007/s40520-021-01942-8 · Cited by 257
The Role of Oxidative Stress in Skeletal Muscle Myogenesis and Muscle Disease
Lian, D., Chen, M.-M., Wu, H., Deng, S., & Hu, X. (2022) · Antioxidants · doi:10.3390/antiox11040755 · Cited by 232
“Moreover mitochondrial regulation of muscle metabolism and mitochondrial dysfunction may play a role in sarcopenia [93].”
BackgroundMolecular Mechanisms of Inflammation in Sarcopenia: Diagnosis and Therapeutic Update
Jiménez-Gutiérrez, G. E., Martínez-Gómez, L. E., Martínez-Armenta, C., Pineda, C., Martínez‐Nava, G. A., & López-Reyes, A. G. (2022) · Cells · doi:10.3390/cells11152359 · Cited by 245
“These mitochondrial changes are major factors that contribute to the age-dependent muscle degeneration observed in sarcopenia [96].”
BackgroundRole of Age-Related Mitochondrial Dysfunction in Sarcopenia
Ferri, E., Marzetti, E., Calvani, R., Picca, A., Cesari, M., & Arosio, B. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21155236 · Cited by 224
“Notably, the accumulation of damaged mitochondria has shown to trigger motor neuron and muscle fiber death, highlighting their relevance in the development of sarcopenia [26].”
BackgroundMeex, R. C. R., Blaak, E. E., & van Loon, L. J. C. (2019) · Obesity Reviews · doi:10.1111/obr.12862 · Cited by 224
“been suggested that accumulation of dysfunctional mitochondria initiate a signalling cascade leading to motor neuron and muscle fibre death and culminating in muscle loss (Figure 2).(127) Not all studies point in the same direction though, and a number of articles raised doubts concerning mitochondrial dysfunction as…”
BackgroundNunes, E. A., Stokes, T., McKendry, J., Currier, B. S., & Phillips, S. M. (2022) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00425.2021 · Cited by 194
Sarcopenia: Etiology, Nutritional Approaches, and miRNAs
Cannataro, R., Carbone, L., Petro, J. L., Cione, E., Vargas-Molina, S., Romero, H. M. A., Forero, D. A., Odriozola-Martínez, A., Kreider, R. B., & Bonilla, D. A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22189724 · Cited by 179
“Thus, the mitochondrial degeneration is associated with impaired energy generation and ROS production, which might be the primary initiators for the resulting alteration of the phenotype in sarcopenia [34,35].”
BackgroundInfluentialSarcopenia and Its Implications for Metabolic Health
Hunter, G. R., Singh, H., Carter, S. J., Bryan, D. R., & Fisher, G. (2019) · Journal of Obesity · doi:10.1155/2019/8031705 · Cited by 156
“Alpha motor neuron death also can occur following oxidative stress with the removal of the neuron nuclei [21].”
BackgroundCarter, H. N., Kim, Y., Erlich, A. T., Zarrin‐khat, D., & Hood, D. A. (2018) · The Journal of Physiology · doi:10.1113/jp275998 · Cited by 136
“Implicated in the maintenance of skeletal muscle with ageing is the presence of a healthy population of mitochondria (Romanello & Sandri, 2016; Rygiel et al. 2016; Alway et al. 2017).”
BackgroundSarcopenia: Current treatments and new regenerative therapeutic approaches
Lo, J. C. Y., Kin Pong, U., Yiu, T. L., Ong, M. T., & Lee, W. (2020) · Journal of Orthopaedic Translation · doi:10.1016/j.jot.2020.04.002 · Cited by 137
“Mitochondria fusion and fission are two different processes with fusion being to process that mitigates stress by mixing contents of partially damaged mitochondria as a form of complementation while the latter being the process necessary to create new mitochondria and contribute to quality control of mitochondria via…”
BackgroundLiu, D., Wang, S., Liu, S., Wang, Q., Che, X., & Wu, G. (2024) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2024.101270 · Cited by 157
Chen, L.-H., Huang, S.-Y., Huang, K.-C., Hsu, C.-C., Yang, K.-C., Li, L.-A., Chan, C.-H., & Huang, H.-Y. (2019) · Aging · doi:10.18632/aging.101782 · Cited by 117
“ROS is another dominant factor leading to mitochondrial dysfunction and sarcopenia [64]; reducing ROS has been shown to improve the sarcopenia resulting from mitochondrial dysfunction [46].”
BackgroundImpact of Melatonin on Skeletal Muscle and Exercise
Stacchiotti, A., Favero, G., & Rodella, L. F. (2020) · Cells · doi:10.3390/cells9020288 · Cited by 116
Luo, Y., Zhou, X., Tian, H., Yang, L., Zhu, Y.-H., Hu, P., & Yao, X. (2024) · Journal of Cachexia Sarcopenia and Muscle · doi:10.1002/jcsm.13541 · Cited by 103
“24 These molecular process include loss of proteostasis, impaired mitochondrial function, neuromuscular remodelling, in fl ammation, apoptotic signalling, among others, 23,25,26 which are core hallmarks of aging.”
BackgroundMitochondria transplant therapy improves regeneration and restoration of injured skeletal muscle
Alway, S. E., Paez, H. G., Pitzer, C. R., Ferrandi, P. J., Khan, M. M., Mohamed, J. S., Carson, J. A., & Deschenes, M. R. (2023) · Journal of Cachexia Sarcopenia and Muscle · doi:10.1002/jcsm.13153 · Cited by 87
Self-citationThe role of SIRT1 in skeletal muscle function and repair of older mice
Myers, M. J., Shepherd, D. L., Durr, A. J., Stanton, D. S., Mohamed, J. S., Hollander, J. M., & Alway, S. E. (2019) · Journal of Cachexia Sarcopenia and Muscle · doi:10.1002/jcsm.12437 · Cited by 87
“There is likely a link between mitochondrial dysfunction and aging(53) including sarcopenia.(4) As SIRT1 is a known regulator of PGC1α which in turn regulates mitochondria biogenesis, we next decided to investigate the effects that SIRT1 expression levels had on mitochondrial activity in the skeletal”
BackgroundSelf-citationLiang, J., Zhang, H., Zeng, Z., Wu, L., Zhang, Y., Guo, Y., Lv, J., Wang, C., Fan, J., & Chen, N. (2021) · Metabolites · doi:10.3390/metabo11050323 · Cited by 84
“To cope with these changes, mitophagy, as a kind of selective autophagy, can identify and degrade damaged and dysfunctional mitochondria, thus generating a self-protective coping mechanism against mitochondrial dysfunction [47].”
BackgroundMitochondrial Mechanisms of Neuromuscular Junction Degeneration with Aging
Anagnostou, M., & Hepple, R. T. (2020) · Cells · doi:10.3390/cells9010197 · Cited by 84
Potential roles of vitamin E in age-related changes in skeletal muscle health
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Exercise and mitochondrial mechanisms in patients with sarcopenia
Pahlavani, H. A., Laher, I., Knechtle, B., & Zouhal, H. (2022) · Frontiers in Physiology · doi:10.3389/fphys.2022.1040381 · Cited by 76
“the outer mitochondria membrane (OMM) provides an important mechanism for identifying damaged mitochondria (Alway et al., 2017).”
BackgroundCrupi, A. N., Nunnelee, J. S., Taylor, D. J., Thomas, A., Vit, J., Riera, C. E., Gottlieb, R. A., & Goodridge, H. S. (2018) · Aging · doi:10.18632/aging.101643 · Cited by 72
“In this context, our study provides possible mechanistic explanations for recent findings related to the anti-aging effects of physical exercise on skeletal muscle [61-63] and further reinforces the idea that exercise training aimed at improving oxidative metabolism may be the most complete and direct approach to prev…”
BackgroundDrug-Induced Mitochondrial Toxicity in the Geriatric Population: Challenges and Future Directions
Will, Y., Shields, J. E., & Wallace, K. B. (2019) · Biology · doi:10.3390/biology8020032 · Cited by 65
“Mitochondrial dysfunction is implicated i many age-relat d diseases such as metabolic diseases (T2DM, obesity, ardiovascula and cerebrovascular disease, Non-Alcoholic Fatty Liver Disease (NAFDL)) [2–7], CNS-r lated diseases (Parkinson’s, Alzheimer’s and Huntington’s disease, he ring loss, cataracts) [8–11], inflammati…”
BackgroundAn Integrated Approach to Skeletal Muscle Health in Aging
Agostini, D., Gervasi, M., Ferrini, F., Bartolacci, A., Stranieri, A., Piccoli, G., Barbieri, E., Sestili, P., Patti, A., Stocchi, V., et al. (2023) · Nutrients · doi:10.3390/nu15081802 · Cited by 81
“Oxidative stress is one of the causes of sarcopenia [21], and aging increases the production of ROS [22] and lowers the levels of antioxidant enzymes in muscle and neuronal cells [23] by damaging cellular mitochondria [24].”
BackgroundSkeletal muscle and childhood cancer: Where are we now and where we go from here
Goodenough, C. G., Partin, R. E., & Ness, K. K. (2021) · Aging and Cancer · doi:10.1002/aac2.12027 · Cited by 65
Paez, H. G., Pitzer, C. R., & Alway, S. E. (2023) · Cells · doi:10.3390/cells12020249 · Cited by 71
“tion of the motor neuron is a known contributor to the development of sarcopenia [126].”
InfluentialSelf-citationFan, J., Fan, J., & Khanzada, Z. (2025) · Muscles · doi:10.3390/muscles4030026 · Cited by 65
“…including muscle stem cell (satellite cell) dysfunction, neuromuscular junction (NMJ) instability, and chronic low-grade inflammaging (also known as inflammation)—all of which contribute to the initiation and progression of muscle deterioration with age and muscle related diseases [13,15–19].”
Ageing of skeletal muscle extracellular matrix and mitochondria: finding a potential link
Cai, L., Shi, L., Peng, Z., Sun, Y., & Chen, J. (2023) · Annals of Medicine · doi:10.1080/07853890.2023.2240707 · Cited by 63
“For instance, the ability of mitochondrial ATP production declined in elder adults [14], and the accumulation of impaired mitochondria may play a part in muscle fibre death [15].”
BackgroundMitochondrial Quality Control in Sarcopenia: Updated Overview of Mechanisms and Interventions
Liu, D., Fan, Y., Tao, X., Pan, W., Wu, Y., Wang, X., He, Y., Xiao, W., & Li, Y. (2021) · Aging and Disease · doi:10.14336/ad.2021.0427 · Cited by 62
“Adverse alternations in the quality control mechanisms may lead to mitochondrial dysfunction, which can further contribute to muscle wasting and even sarcopenia [22-25].”
BackgroundImpacts of Green Tea on Joint and Skeletal Muscle Health: Prospects of Translational Nutrition
Luk, H., Appell, C. R., Chyu, M., Chen, C., Wang, C., Yang, R., & Shen, C. (2020) · Antioxidants · doi:10.3390/antiox9111050 · Cited by 60
Qaisar, R., Pharaoh, G. A., Bhaskaran, S., Xu, H., Ranjit, R., Bian, J., Ahn, B., Georgescu, C., Wren, J. D., & Remmen, H. V. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms22010037 · Cited by 57
From mitochondria to sarcopenia: role of 17β-estradiol and testosterone
Tian, X., Lou, S., & Shi, R. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1156583 · Cited by 54
“Figure 1 shows the general pathways initiated by mitochondrial alteration resulting in motor neuron and muscle cell death and culminating in sarcopenia (14).”
BackgroundOliveira, J. R. S., Mohamed, J. S., Myers, M. J., Brooks, M. J., & Alway, S. E. (2018) · Experimental Gerontology · doi:10.1016/j.exger.2018.11.011 · Cited by 52
“…associated changes in apoptosis and autophagy have been proposed to have roles in muscle atrophy and reduced muscle recovery after HLS in aged rats (Alway, 2017; Alway et al., 2015; Alway et al., 2017a; Alway et al. 2017c; Baehr et al., 2016; Baehr et al., 2017; Cannavino et al., 2015; Takahashi…”
Self-citationBrooks, M. J., Hajira, A., Mohamed, J. S., & Alway, S. E. (2018) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00451.2017 · Cited by 52
“A novel finding of our study was that wheel running during reloading improved the oxidative phenotype of the gastrocnemius muscle, providing a likely mechanism to explain the enhanced resistance to fatigue and perhaps improved muscle recovery as a result of lower death signaling during the reloading period (4).”
BackgroundSelf-citationAcute Sarcopenia: Mechanisms and Management
Damanti, S., Senini, E., LORENZO, R. D., Merolla, A., Santoro, S., Festorazzi, C., Messina, M., Vitali, G., Sciorati, C., & Rovere, P. Q. (2024) · Nutrients · doi:10.3390/nu16203428 · Cited by 53
Advances in sarcopenia: mechanisms, therapeutic targets, and intervention strategies
Zheng, Y., Feng, J., Yu, Y., Ling, M., & Wang, X. (2024) · Archives of Pharmacal Research · doi:10.1007/s12272-024-01493-2 · Cited by 46
“Importantly, the buildup of dysfunctional mitochondria has been linked to the initiation of motor neuron and muscle fiber death, underscoring their significance in the advancement of sarcopenia (Alway et al. 2017b; Wang et al. 2022).”
McKendry, J., Coletta, G., Nunes, E. A., Lim, C., & Phillips, S. M. (2024) · Experimental Physiology · doi:10.1113/ep091937 · Cited by 47
Targeting mitochondrial quality control for treating sarcopenia: lessons from physical exercise
Picca, A., Calvani, R., Leeuwenburgh, C., Coelho‐Júnior, H. J., Bernabei, R., Landi, F., & Marzetti, E. (2018) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2019.1559827 · Cited by 43
Skeletal Muscle Metabolic Alternation Develops Sarcopenia
Yang, Q., & Chan, P. (2022) · Aging and Disease · doi:10.14336/ad.2021.1107 · Cited by 50
“1) is related to decreased neuro-muscular function [5-7], proinflammatory cytokines [8-10], imbalance of calcium homeostasis [11], imbalance in protein synthesis and decomposition [12], changes in caloric and protein intake[13], changes in hormone levels [14-17], mitochondrial dysfunction[18-20], free radical oxidativ…”
BackgroundThe Role of Mitochondria in Mediation of Skeletal Muscle Repair
Alway, S. E., Paez, H. G., & Pitzer, C. R. (2023) · Muscles · doi:10.3390/muscles2020011 · Cited by 48
“Premature or prolonged opening of the mPTP releases the mitochondrial contents to the cytoplasm, and this can amplify ROS and induce apoptosis [46,390,391].”
BackgroundInfluentialSelf-citationCirculating Mediators of Apoptosis and Inflammation in Aging; Physical Exercise Intervention
Morawin, B., Tylutka, A., Chmielowiec, J., & Zembroń-Łacny, A. (2021) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph18063165 · Cited by 42
“However, the exact molecular and cellular mechanisms underlying the loss of muscle mass in the elderly are still largely unknown [12].”
BackgroundThe Current Landscape of Pharmacotherapies for Sarcopenia
Bahat, G., & Özkök, S. (2024) · Drugs & Aging · doi:10.1007/s40266-023-01093-7 · Cited by 41
“2) [72].”
Takahashi, H., Suzuki, Y., Mohamed, J. S., Gotoh, T., Pereira, S. L., & Alway, S. E. (2017) · Experimental Gerontology · doi:10.1016/j.exger.2017.02.075 · Cited by 37
Self-citationPhysiological Systems in Promoting Frailty
Perazza, L. R., Brown‐Borg, H. M., & Thompson, L. V. (2022) · Comprehensive physiology · doi:10.1002/cphy.c210034 · Cited by 69
“…of deficits in protein quality control (e.g., increased levels of heat shock proteins, protein modifications, lipofuscin, misfolded proteins, aggregation, impaired mitophagy/autophagy), which contribute to reductions in muscle quantity and quality with aging and MetSs (Figure 7) (1, 11, 206, 430).”
Skawratananond, S., Xiong, D. X., Zhang, C., Tonk, S. S., Pinili, A., Delacruz, B., Pham, P., Smith, S. C., Navab, R., & Reddy, P. H. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102732 · Cited by 41
Sonjak, V., Jacob, K. J., Spendiff, S., Vuda, M., Pérez, A., Míguez, K., Minozzo, F. C., Spake, C. S. L., Morais, J. A., & Hepple, R. T. (2019) · The Journals of Gerontology Series A · doi:10.1093/gerona/glz066 · Cited by 34
Extracellular matrix/mitochondria pathway: A novel potential target for sarcopenia
Melouane, A., Yoshioka, M., & St‐Amand, J. (2019) · Mitochondrion · doi:10.1016/j.mito.2019.10.007 · Cited by 35
Pilot Study on Genetic Associations With Age-Related Sarcopenia
Urzi, F., Pokorny, B., & Bužan, E. (2021) · Frontiers in Genetics · doi:10.3389/fgene.2020.615238 · Cited by 36
Exercise is mitochondrial medicine for muscle
Oliveira, A. N., & Hood, D. A. (2019) · Sports Medicine and Health Science · doi:10.1016/j.smhs.2019.08.008 · Cited by 37
Sarcopenia: investigation of metabolic changes and its associated mechanisms
Júnior, J. G. M., Shokry, E., Uhl, O., Baber, L., Hofmeister, F., Jarmusch, S., Bidlingmaier, M., Ferrari, U., Koletzko, B. V., & Drey, M. (2023) · Skeletal Muscle · doi:10.1186/s13395-022-00312-w · Cited by 37
“ROS production increases with aging due to the decreased levels of antioxidant enzymes and might be secondary to age muscle denervation [24].”
BackgroundMotanova, E. S., Pirazzini, M., Negro, S., Rossetto, O., & Narici, M. V. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102586 · Cited by 43
Neuromuscular changes of the aged human hamstrings
Kirk, E. A., Gilmore, K. J., & Rice, C. L. (2018) · Journal of Neurophysiology · doi:10.1152/jn.00794.2017 · Cited by 33
“Neuromuscular factors implicated in aging involve changes in motor unit (MU) structure and function (Alway et al. 2017; Hepple and Rice 2016).”
BackgroundRosa‐Caldwell, M. E., Lim, S., Haynie, W. S., Brown, J. L., Lee, D. E., Dunlap, K. R., Jansen, L. T., Washington, T. A., Wiggs, M. P., & Greene, N. P. (2021) · Journal of Cachexia Sarcopenia and Muscle · doi:10.1002/jcsm.12809 · Cited by 32
Advances in exercise to alleviate sarcopenia in older adults by improving mitochondrial dysfunction
Zhu, Y., Zhou, X., Zhu, A., Xiong, S., Xie, J., & Bai, Z. (2023) · Frontiers in Physiology · doi:10.3389/fphys.2023.1196426 · Cited by 34
“As a result, mitochondrial apoptosis and damage to mitochondrial DNA (mtDNA) are increased, mitochondrial calcium (Ca) homeostasis is disrupted, and mitochondrial fusion/fission and mitochondrial biogenesis are inhibited (Chabi et al., 2008; Andersson et al., 2011; Alway et al., 2017).”
BackgroundAli, S. R., Nkembo, A. T., Tipparaju, S. M., Ashraf, M., & Xuan, W. (2024) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/cjpp-2024-0201 · Cited by 37
Nutrition and microRNAs: Novel Insights to Fight Sarcopenia
Barbiera, A., Pelosi, L., Sica, G., & Scicchitano, B. M. (2020) · Antioxidants · doi:10.3390/antiox9100951 · Cited by 32
“The mechanisms that underlie sarcopenia are not yet completely elucidated, but it is likely that sarcopenia is the result of multifactorial events, such as a reduction in number and activity of satellite cells [6], mitochondrial dysfunction [7,8], elevated level of inflammation [9], increased ROS production [10] and i…”
BackgroundSkeletal Muscle Gene Expression in Long-Term Endurance and Resistance Trained Elderly
Bolotta, A., Filardo, G., Abruzzo, P. M., Astolfi, A., Sanctis, P. D., Martino, A. D., Höfer, C., Indio, V., Kern, H., Löfler, S., et al. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21113988 · Cited by 30
“Several combined factors underlie the establishment of sarcopenia, including a decline in muscle stem cells [1–5], the occurrence of mitochondrial dysfunction [6,7], hormonal deregulation [8] and the activation of inflammatory signal pathways [9,10].”
BackgroundOxidative pathophysiology following volumetric muscle loss injury in a porcine model
Chao, T., Burmeister, D. M., Corona, B. T., & Greising, S. M. (2019) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00026.2019 · Cited by 26
“Altered mitochondrial function in skeletal muscle has been implicated in other diseases and injuries such as cancer cachexia (2, 4, 21) and age-related sarcopenia (1, 20, 22).”
BackgroundKoo, J., Kang, E., & Cho, J. (2019) · Gerontology · doi:10.1159/000494723 · Cited by 24
Efficient clofilium tosylate-mediated rescue of POLG-related disease phenotypes in zebrafish
Facchinello, N., Laquatra, C., Locatello, L., et al. (2021) · Cell Death and Disease · doi:10.1038/s41419-020-03359-z · Cited by 24
Resveratrol and Vitamin D: Eclectic Molecules Promoting Mitochondrial Health in Sarcopenia
Russo, C., Valle, M. S., D’Angeli, F., Surdo, S., & Malaguarnera, L. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25147503 · Cited by 27
“This results in mitochondrial damage and dysfunction in both muscle and nerve cells [92].”
BackgroundLong, Y., Chow, S. K., Cui, C., Wong, R. M. Y., Qin, L., Law, S. W., & Cheung, W. (2022) · Journal of Orthopaedic Translation · doi:10.1016/j.jot.2022.06.003 · Cited by 23
“ROS are kinds of metabolite produced by mitochondria during oxidative phosphorylation when it utilizes oxygen to generate ATP [38] that is regarded as one of the factors leading to sarcopenia during ageing via disrupting mitochondrial function [39,40].”
BackgroundZhang, W., You, B., Qi, D., Qiu, L., Ripley-Gonzalez, J. W., Zheng, F., Fu, S., Li, C., Dun, Y., & Liu, S. (2021) · Scientific Reports · doi:10.1038/s41598-021-98771-6 · Cited by 22
Mitochondrial transplantation as a possible therapeutic option for sarcopenia
Türkel, İ., Özerkliğ, B., Yılmaz, M., Ülger, Ö., Kubat, G. B., & Tuncer, M. (2023) · Journal of Molecular Medicine · doi:10.1007/s00109-023-02326-3 · Cited by 25
Papadopoulos, E., Irving, B. A., Brown, J. C., Heymsfield, S. B., Sattar, S., Alibhai, S. M. H., Williams, G. R., & Dunne, R. F. (2025) · Drugs & Aging · doi:10.1007/s40266-025-01252-y · Cited by 28
“Mitochondrial dysfunction is also implicated in the development of age-related sarcopenia [116, 117].”
Serum GDF15 Level Is Independent of Sarcopenia in Older Asian Adults
Nga, H. T., Jang, I., Kim, D. A., Park, S. J., Lee, J. Y., Lee, S., Kim, J. H., Lee, E., Park, J. H., Lee, Y., et al. (2021) · Gerontology · doi:10.1159/000513600 · Cited by 22
Ciarambino, T., Crispino, P., Minervini, G., & Giordano, M. (2023) · Vaccines · doi:10.3390/vaccines11030606 · Cited by 25
“Muscle, as a tissue with a high energy turnover, has a large pool of mitochondria that would make muscle fibers more susceptible to ROS damage and autophagy in the event of COVID-19 infection [30,31].”
BackgroundMolecular and Structural Alterations of Skeletal Muscle Tissue Nuclei during Aging
Cisterna, B., & Malatesta, M. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25031833 · Cited by 27
“…such as the loss of protein homeostasis, along with the impairment of proteolytic and autophagic pathways [15–18], mitochondrial dysfunction [19,20], the depletion of myofiber nuclei [21–23], a reduced number of satellite cells and/or the alteration of their proliferation and differentiation…”
BackgroundMyers, M. J., Shaik, F., Shaik, F., Alway, S. E., & Mohamed, J. S. (2021) · Genes · doi:10.3390/genes12050691 · Cited by 19
“SirT1 OE in the present study inhibited pathways linked to apoptosis [72,73].”
BackgroundSelf-citationMitochondria Transplantation from Stem Cells for Mitigating Sarcopenia
Tian, X., Pan, M., Zhou, M., Tang, Q., Chen, M., Hong, W., Zhao, F., & Liu, K. (2023) · Aging and Disease · doi:10.14336/ad.2023.0210 · Cited by 18
Yu, J., Loh, K., Yang, H.-Q., Du, M.-R., Wu, Y.-X., Liao, Z., Guo, A., Yang, Y., Chen, B., Zhao, Y., et al. (2022) · Communications Biology · doi:10.1038/s42003-022-03728-8 · Cited by 17
Aldrich, L., Ispoglou, T., Prokopidis, K., Alqallaf, J., Wilson, O. J., & Stavropoulos‐Kalinoglou, A. (2024) · Journal of Cachexia Sarcopenia and Muscle · doi:10.1002/jcsm.13662 · Cited by 20
Integrating Mechanisms of Exacerbated Atrophy and Other Adverse Skeletal Muscle Impact in COPD
Taivassalo, T., & Hepple, R. T. (2022) · Frontiers in Physiology · doi:10.3389/fphys.2022.861617 · Cited by 16
“It is important to point out that these mitochondrial alterations exceed those already occurring with normal aging in skeletal muscle, and the reader is directed to a recent review of this latter topic (Alway et al., 2017).”
BackgroundLee, M. J.-C., Saner, N. J., Ferri, A., García-Domínguez, E., Broatch, J. R., & Bishop, D. J. (2024) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2024.101272 · Cited by 18
MicroRNAs as the Sentinels of Redox and Hypertrophic Signalling
Kolodziej, F., McDonagh, B., Burns, N. C., & Goljanek‐Whysall, K. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232314716 · Cited by 15
Zhou, P., She, M., Liu, P., Zhang, S., & Li, J. (2020) · Sensors and Actuators B Chemical · doi:10.1016/j.snb.2020.128258 · Cited by 15
The role of melatonin in sarcopenia: Advances and application prospects
Jin, H., Xie, W., Hu, P., Tang, K., Wang, X., Wu, Y., He, M., Yu, D., & Li, Y. (2021) · Experimental Gerontology · doi:10.1016/j.exger.2021.111319 · Cited by 16
Zou, Y., Tang, X., Yang, S., Chen, Z., Liu, B., 周作琼, Peng, X., & Tang, C. (2024) · Metabolism · doi:10.1016/j.metabol.2024.155972 · Cited by 14
Exerkines and myokines in aging sarcopenia
Wang, H., He, W., Chen, P., Wang, H., Wang, H., Zhu, L., & Liu, X. (2025) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1592491 · Cited by 20
“Finally, mitochondria play a crucial role in muscle mass and function, and their dysfunction is a driver of sarcopenia (29, 31 – 33).”
Identification of the cuproptosis-related hub genes and therapeutic agents for sarcopenia
Zhu, Y., Chen, X., Geng, S., Li, Q., Li, Y., Yuan, H., & Jiang, H. (2023) · Frontiers in Genetics · doi:10.3389/fgene.2023.1136763 · Cited by 16
“The GO molecular function terms also highlighted their important roles in oxidoreductase activity, catalytic activity as well as NADH dehydrogenase activity, which is consistent with the perspective of earlier studies that dysfunctional mitochondria play a key role in initiating and exacerbating sarcopenia (Alway et a…”
BackgroundResultMitochondrial Dysfunction: Linking Type 1 Diabetes and Sarcopenia
Alway, S. E. (2019) · Exercise and Sport Sciences Reviews · doi:10.1249/jes.0000000000000186 · Cited by 13
“In their model (1), loss of mitochondrial function in T1D (2,3) is similar to that which occurs in aging (4).”
BackgroundSelf-citationDirect or indirect regulation of muscle protein synthesis by energy status?
Moinard, C., & Fontaine, E. M. (2020) · Clinical Nutrition · doi:10.1016/j.clnu.2020.07.015 · Cited by 12
García-Casas, P., Álvarez-Illera, P., Gómez‐Orte, E., Cabello, J., Fonteríz, R. I., Montero, M., & Álvarez, J. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.695687 · Cited by 11
“Moreover, it has been recently postulated that mitochondrial deterioration inmuscle andmotor neurons is the primary initiator of sarcopenia and that interventions aimed at improvingmitochondrial function and proteostatic maintenance could mitigate or treat this process of muscle loss (Alway et al., 2017; Coen et al.,…”
BackgroundChen, Q., Huang, W., Çapanoğlu, E., Amrouche, A. T., & Lu, B. (2023) · Food Frontiers · doi:10.1002/fft2.261 · Cited by 12
Wang, M., Wu, X., Jiao, Y., Yin, W., & Zhang, L. (2024) · Aging and Disease · doi:10.14336/ad.2024.0318 · Cited by 11
“[11].”
Sarcopenia in chronic liver diseases: a translational overview
Barbero-Becerra, V. J., López-Méndez, I., Romo‐Araiza, A., Visag-Castillo, V., Chávez-Tapia, N. C., Uribe, M., & Juárez-Hernández, E. (2020) · Expert Review of Gastroenterology & Hepatology · doi:10.1080/17474124.2020.1757427 · Cited by 11
“opening, which initiates a signaling cascade leading to motor neuron and muscle fiber apoptosis and culminating in sarcopenia [9].”
BackgroundBerberine suppressed sarcopenia insulin resistance through SIRT1-mediated mitophagy
Su, X., Yang, D., Hu, Y., Yuan, Y., & Song, L. (2023) · Open Life Sciences · doi:10.1515/biol-2022-0648 · Cited by 11
“It was aware of that sarcopenia and insulin resistance were related to mitochondria function mitochondria [26].”
BackgroundEffects of Aging on Metabolic Characteristics of Human B Cells
Frasca, D., Pallikkuth, S., & Pahwa, S. G. (2022) · JAIDS Journal of Acquired Immune Deficiency Syndromes · doi:10.1097/qai.0000000000002860 · Cited by 10
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Teo, W., Lo, J., Fann, Y., Huang, C., & Huang, T.-F. (2020) · PLoS ONE · doi:10.1371/journal.pone.0244791 · Cited by 10
Hydrangea serrata Tea Enhances Running Endurance and Skeletal Muscle Mass
Jang, Y. J., Ahn, J., Son, H. J., Jung, C. H., Ahn, J., & Ha, T. Y. (2019) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.201801149 · Cited by 10
What Does Sarcopenia Have to Do with Nonalcoholic Fatty Liver Disease?
Ferenc, K., Jarmakiewicz-Czaja, S., & Filip, R. (2023) · Life · doi:10.3390/life14010037 · Cited by 10
Cellular and Mitochondrial Quality Control Mechanisms in Maintaining Homeostasis in Aging
Langeh, U., Kumar, V., Kumar, A., Kumar, P., Singh, C., & Singh, A. (2022) · Rejuvenation Research · doi:10.1089/rej.2022.0027 · Cited by 9
“The balance of fusion, fission, and mitophagy is required for normal cellular activities, however, the disturbances in these processes result in decreased production of ATP (one of the hallmarks of aging) 25 (Fig.”
Zhang, X., Liao, S., Huang, L., & Wang, J. (2024) · Advanced Biology · doi:10.1002/adbi.202400235 · Cited by 11
Paez, H. G., Pitzer, C. R., Halle, J. L., Ferrandi, P. J., Carson, J. A., Mohamed, J. S., & Alway, S. E. (2025) · GeroScience · doi:10.1007/s11357-025-01726-2 · Cited by 9
“Aging is associated with motor unit loss [4], altered proteostasis [5], mitochondrial dysfunction [6, 7], systemic inflammation [8], and inflammasome activation in skeletal muscle [9].”
Self-citationDamanti, S., Sciorati, C., LORENZO, R. D., Avola, A., Ruggiero, M. P., Santoro, S., Senini, E., Messina, M., Farina, F., Festorazzi, C., et al. (2025) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2025.112124 · Cited by 13
Carbon monoxide-loaded cell therapy as an exercise mimetic for sarcopenia treatment
Noguchi, I., Maeda, H., Kobayashi, K., Nagasaki, T., Kato, H., Yanagisawa, H., Wada, N., Kanazawa, G., Kaji, T., Sakai, H., et al. (2024) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2024.04.231 · Cited by 10
Gicquel, T., Marchianò, F., Reyes‐Castellanos, G., Audebert, S., Camoin, L., Habermann, B. H., Giannesini, B., & Carrier, A. (2024) · eLife · doi:10.7554/elife.93312.2 · Cited by 24
Alcohol Alters Skeletal Muscle Bioenergetic Function: A Scoping Review
DiLeo, M. R., Hall, R. E., Vellers, H. L., Daniels, C. L., & Levitt, D. E. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252212280 · Cited by 7
“For example, SKM mitochondrial dysfunction contributes to sarcopenia development [18].”
Metadata
- Authors
- Alway, S. E., Mohamed, J. S., & Myers, M. J.
- Affiliations
- West Virginia University (US)
- Corresponding author
- Alway, Stephen E.
- Venue
- Exercise and Sport Sciences Reviews
- Published
- 2017-04
- Volume
- 45
- Issue
- 2
- Pages
- 58-69
- ISSN
- 0091-6331 (ISSN-L)
- 1538-3008
- PMC
- PMC5357179
- OpenAlex
- W2576104985
- Semantic Scholar
- a327c586451d76c3458f3b2dcee83eaa79f8426b
- Cited by
- 153
- References
- 151
- Citations by year
- 2026: 10 · 2025: 24 · 2024: 24 · 2023: 22 · 2022: 17 · 2021: 17 · 2020: 16 · 2019: 13 · 2018: 8 · 2017: 2
- FWCI
- 1.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Exercise and Sport Sciences Reviews (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- The Research Repository @ WVU (West Virginia University) (submittedVersion)
- Funders
- West Virginia University
- National Institutes of Health (2p20rr016477-09, 1p30rr032138-01)
- National Institute of General Medical Sciences (P30GM103488, P20GM103434, U54GM104942)
- National Center for Research Resources (P30-RR-032138, P20-RR016477, P20RR016440)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology (medical) › Nutrition and Health in Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- sarcopenia, mitochondrial dysfunction, motor neuron degeneration, signaling pathways, sarcopenia prevention
- MeSH terms
- Forkhead Box Protein O1, Aging, Animals, Humans, Mitochondria, Muscle, Motor Neurons, Muscular Atrophy, Signal Transduction, Cell Death, Apoptosis, Muscle, Skeletal, Ubiquitin, Sarcopenia, Mitophagy
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