The DOI matches its Crossref record; 60 of the 60 references it cites were found in a registry or an index; 6 of the 98 sources its claims cite were checked for support.
Impaired mitophagy leads to cigarette smoke stress‐induced cellular senescence: implications for chronic obstructive pulmonary disease
Open accessAbstract
Cigarette smoke (CS)‐induced cellular senescence is involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). The molecular mechanism by which CS induces cellular senescence is unknown. Here, we show that CS stress (exposure of primary lung cells to CS extract 0.2‐0.75% with a half‐maximal inhibitory concentration of ~0.5%) led to impaired mitophagy and perinuclear accumulation of damaged mitochondria associated with cellular senescence in both human lung fibroblasts and small airway epithelial cells (SAECs). Impaired mitophagy was attributed to reduced Parkin translocation to damaged mitochondria, which was due to CS‐induced cytoplasmic p53 accumulation and its interaction with Parkin. Impaired Parkin translocation to damaged mitochondria was also observed in mouse lungs with emphysema (6 months CS exposure, 100 mg TPM/m 3 ) as well as in lungs of chronic smokers and patients with COPD. Primary SAECs from patients with COPD also exhibited impaired mitophagy and increased cellular senescence via suborganellar signaling. Mitochondria‐targeted antioxidant (Mito‐Tempo) restored impaired mitophagy, decreased mitochondrial mass accumulation, and delayed cellular senescence in Parkin‐overexpressing cells. In conclusion, defective mitophagy leads to CS stress‐induced lung cellular senescence, and restoring mitophagy delays cellular senescence, which provides a promising therapeutic intervention in chronic airway diseases.—Ahmad, T., Sundar, I. K., Lerner, C. A., Gerloff, J., Tormos, A. M., Yao, H., Rahman, I. Impaired mitophagy leads to cigarette smoke stress‐induced cellular senescence: implications for chronic obstructive pulmonary disease. FASEB J . 29, 2912‐2929 (2015). www.fasebj.org
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TL;DR
Cigarette smoke stress impairs mitophagy in lung fibroblasts and small airway epithelial cells, leading to perinuclear accumulation of damaged mitochondria, DNA damage, and cellular senescence. Restoring Parkin-mediated mitophagy together with mitochondria-targeted antioxidant treatment delays senescence, suggesting a therapeutic target in COPD.
Key findings
- CSE exposure (0.2–0.75%; half-maximal inhibitory concentration ∼0.5%) induced cellular senescence in human lung fibroblasts and SAECs, with increased SA-β-gal/C12FDG, p16, p21, γ-H2AX foci, mtROS, mitochondrial mass, and decreased ATP.
- Impaired mitophagy was attributed to reduced Parkin translocation to damaged mitochondria, linked to CS-induced cytoplasmic p53 accumulation and its interaction with Parkin; Pink1 was stabilized on mitochondria, Mfn2 increased, and Drp1 showed more cytoplasmic localization with a slight decrease.
- Impaired Parkin mitochondrial translocation was also seen in mouse lungs with emphysema after 6 months CS exposure (100 mg TPM/m3), in lungs of chronic smokers and patients with COPD, and in primary SAECs from patients with COPD, which showed increased mitochondrial mass and senescence augmented by CSE.
- Parkin overexpression restored mitophagy and reduced mitochondrial mass; in Parkin-overexpressing cells, Mito-Tempo (1 µM) reduced mtROS, perinuclear mitochondrial accumulation, γ-H2AX foci, and delayed cellular senescence. MitoT alone reduced mtROS but did not rescue impaired mitophagy or senescence.
Methods
- In vitro models used human lung fibroblasts (HFL1, WI-38 LC3-GFP), primary mouse lung fibroblasts, and human primary SAECs from nonsmokers and patients with COPD; CSE was used at 0.2–0.75%, with 0.5% for HFL1, 0.25% for mouse lung fibroblasts, and 0.2% for human SAECs, over 10–15 days with alternate-day treatment.
- In vivo/ex vivo samples included 8-week-old C57BL/6J mice exposed to CS 5 h/day, 5 days/week for 6 months at ∼100 mg/m3 total particulate matter, and human lung tissue from normal nonsmokers, smokers, and patients with COPD.
- Assays included SA-β-gal, C12FDG flow cytometry, immunofluorescence/confocal microscopy, electron microscopy, MitoTracker Green/Red, MitoSOX, TMRM, mitochondrial ATP, γ-H2AX foci, CellROX, Western blot, mitochondrial isolation, and 1-way ANOVA with means ± SEM.
Limitations
- Stated: long-term nocodazole treatment caused cell death, so the effect of perinuclear mitochondrial accumulation on cellular senescence could not be directly evaluated; Parkin was transiently overexpressed while CSE treatment continued for 15 days; MitoT alone had no significant effect on senescence, possibly due to insufficient concentration/duration; further studies are needed with stable Parkin overexpression, Parkin knockout mice, in vivo MitoT, other lung cell types, and transmitophagy.
- Evident from the text: much of the mechanistic evidence is in vitro, while human COPD/smoker data are tissue associations rather than causal in vivo experiments; mitophagy is assessed mainly by Parkin translocation and LC3 colocalization rather than direct flux measurements; no in vivo rescue with MitoT or Parkin is reported.
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100 Own result · 40 Not checked yet · 33 Own interpretation · 3 Own method · 2 Partly supported · 2 No basis given · accuracy not yet measured
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Mitochondria-targeted antioxidant (Mito-Tempo) restored impaired mitophagy, decreased mitochondrial mass accumulation, and delayed cellular senescence in Parkin-overexpressing cells.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Primary SAECs from patients with COPD also exhibited impaired mitophagy and increased cellular senescence via suborganellar signaling.”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Mitochondria-targeted antioxidant (Mito-Tempo) restored impaired mitophagy, decreased mitochondrial mass accumulation, and delayed cellular senescence in Parkin-overexpressing cells.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Imaging studies revealed an increased nuclear ROS with CSE treatment, although most of the ROS showed a cytoplasmic localization in control untreated cells (Fig. 2G, H).”
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In the paper
“CCCP (catalog number C2759; Sigma-Aldrich) treatment could not induce LC3-GFP association with mitochondria in cells treated with a combination of rotenone and Mdivi-1 (Fig. 4E, F).”
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In the paper
“We show that CSE causes persistent mitochondrial dysfunction leading to defective mitophagy by altering Parkin levels and translocation.”
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“However, Parkin (catalog number 2132S; Cell Signaling Technology) mitochondrial translocation was highly impaired in HFL1 cells by CSE (Fig. 3A, B).”
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In the paper
“Our results show increased p16 and p21 levels (Fig. 1C)”
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In the paper
“Impaired Parkin translocation to damaged mitochondria was also observed in mouse lungs with emphysema (6 months CS exposure, 100 mg TPM/m3) as well as in lungs of chronic smokers and patients with COPD.”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“A time-dependent increase in cellular senescence was observed in HFL1 and mouse primary lung fibroblasts, which was characterized by increased SA-β-gal activity (Fig. 1A and Supplemental Fig. S1A, B).”
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- Probably not a substantial claim. 28
- It may state two separate claims as one. 50
- The quote only partly states this claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Defective mitophagy has also been linked with premature aging and many age-associated disorders, such as Alzheimer’s and Parkinson’s diseases (25–28).”
What the sources say
- Partly supportedcites [25] Chistiakov D. A., Sobenin I. A., Revin V. V., Orekhov A. N., Bobryshev Y. V. (2014) Mitochondrial aging and age-related dysfunction of mitochondria. Biomed Res. Int. 2014, 238463. [DOI] [PMC free article] [PubMed] [Google Scholar] sourceExperimental — accuracy not yet measured
Section 4, “Age-Dependent Changes in Mitochondrial Dynamics” (page not supplied), reports that mitophagy declines with age and associates that decline with damaged mitochondria, oxidative stress, and apoptosis. It does not link defective mitophagy to premature aging or to Alzheimer’s or Parkinson’s disease. Section 2 attributes premature-aging phenotypes to mtDNA mutations in mice, not to defective mitophagy. (LLM, conf=0.86)
- Could not verifycites [26] Bratic A., Larsson N. G. (2013) The role of mitochondria in aging. J. Clin. Invest. 123, 951–957 [DOI] [PMC free article] [PubMed] [Google Scholar] sourceExperimental — accuracy not yet measured
The section ‘Are mtDNA mutations a driving force in aging?’ links premature-aging phenotypes in mice to mtDNA mutations, not defective mitophagy. Searches for mitophagy, mitochondrial autophagy, and Alzheimer’s or Parkinson’s disease found no passage in our copy linking defective mitophagy to the claimed outcomes. (LLM, conf=0.74)
- Partly supportedcites [27] Hoshino A., Mita Y., Okawa Y., Ariyoshi M., Iwai-Kanai E., Ueyama T., Ikeda K., Ogata T., Matoba S. (2013) Cytosolic p53 inhibits Parkin-mediated mitophagy and promotes mitochondrial dysfunction in the mouse heart. Nat. Commun. 4, 2308 [DOI] [PubMed] [Google Scholar] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) links deficient Parkin-mediated mitophagy to aging-related cardiac decline and discusses Parkinson-associated Parkin mutations that impair mitophagy. The introduction mentions premature aging in mice with defects in mitochondrial DNA quality control, but does not establish that defective mitophagy caused it. Our copy does not link defective mitophagy to Alzheimer’s disease. (LLM, conf=0.84)
- Partly supportedcites [28] Bernhardt D., Müller M., Reichert A. S., Osiewacz H. D. (2015) Simultaneous impairment of mitochondrial fission and fusion reduces mitophagy and shortens replicative lifespan. Sci. Rep. 5, 7885 [DOI] [PMC free article] [PubMed] [Google Scholar] sourceExperimental — accuracy not yet measured
The Results (page unavailable) link reduced mitophagy in a yeast mutant to shortened replicative lifespan, supporting an aging-related link. The paper does not establish a link between defective mitophagy and Alzheimer’s or Parkinson’s disease; the diseases named in its Discussion (page unavailable) concern impaired mitochondrial fission or fusion instead. (LLM, conf=0.88)
plaincorrelational- 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This is corroborated by our findings that either Mdivi-1 (mitophagy inhibitor) (49) or rotenone (increasing mtROS generation) (35) induced perinuclear accumulation of damaged mitochondria and cellular senescence.”
What the sources say
- Could not verifycites [49] Gomes L. C., Di Benedetto G., Scorrano L. (2011) During autophagy mitochondria elongate, are spared from degradation and sustain cell viability. Nat. Cell Biol. 13, 589–598 [DOI] [PMC free article] [PubMed] [Google Scholar] sourceExperimental — accuracy not yet measured
The citation is attached to the description of Mdivi-1 as a mitophagy inhibitor; the sentence presents the senescence finding as the citing authors’ own. Our copy’s Results section discusses mitochondrial degradation during starvation and Drp1-deficient cells, but the searched passages contain no Mdivi-1, rotenone, or cellular-senescence result. It therefore does not verify either the drug description or the quoted senescence claim. (LLM, conf=0.76)
- Supportedcites [35] Ahmad T., Aggarwal K., Pattnaik B., Mukherjee S., Sethi T., Tiwari B. K., Kumar M., Micheal A., Mabalirajan U., Ghosh B., Sinha Roy S., Agrawal A. (2013) Computational classification of mitochondrial shapes reflects stress and redox state. Cell Death Dis. 4, e461 [DOI] [PMC free article] [PubMed] [Google Scholar] source
The citation to this paper is attached to the parenthetical description of rotenone as increasing mtROS, not to the citing authors’ statement that their experiments found cellular senescence. The Discussion reports using rotenone to elevate mtROS generation in human lung epithelial cells; it does not report rotenone-induced senescence. (LLM, conf=0.87)
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- Could not verify
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In the paper
“whereas bafilomycin treatment induced more mitochondria fragmentation, and long-term bafilomycin treatment led to cell death rather than cellular senescence (Supplemental Fig. S2G, J).”
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In the paper
“Treatment of cells with Mdivi-1 led to mitochondrial elongation, mitochondrial mass accumulation (Fig. 4A, B), and an increase in cellular senescence (Fig. 4C)”
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“Treatment of cells with CCCP induced a Parkin-dependent mitophagy, as evident by LC3-GFP colocalization in control cells, but not in CSE-treated cells with cellular senescence (Fig. 3G, H).”
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“CSE treatment resulted in a decrease in ΔΨm (Fig. 2A) and showed increased stabilization of Pink1 (catalog number 6946S; Cell Signaling Technology) on mitochondria.”
plaindirect- Asserted: passes — The authors put it forward as true.
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“Confocal microscopy imaging revealed an increase in mitochondrial mass and formation of highly elongated mitochondria after CSE treatment (Fig. 1G)”
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“Time kinetic data revealed a close correlation among mitochondrial mass accumulation, mtROS, ΔΨm, and cellular senescence during CSE treatment (Fig. 2A).”
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In the paper
“Furthermore, levels of Mfn2 (catalog number 11925; Cell Signaling Technology), a mitochondrial fusion protein, were increased and showed more mitochondrial localization, whereas the mitochondrial fission protein dynamin-related protein-1 (Drp1; catalog number ab56788; Abcam) showed more cytoplasmic localization, although slightly decreased (Fig. 3A, B).”
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“After 24 hours, CSE treatment induced a robust perinuclear mitochondrial accumulation (Fig. 2C, D), with increased mtROS, particularly in the perinuclear region (Fig. 2E, F).”
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“Immunofluorescence staining revealed that mitochondria become highly elongated during the establishment of cellular senescence and increase in mass (Fig. 2B).”
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In the paper
“Impaired mitophagy was also seen in both smokers and patients with COPD as well as in a mouse model of chronic CS-induced emphysema.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In isolated mitochondria, CCCP (a known Parkin mitochondrial translocation agent) treatments resulted in increased Parkin mitochondrial translocation in control cells, whereas CCCP-induced Parkin mitochondrial translocation was highly reduced in CSE-treated HFL1 cells (Fig. 3E, F), indicating impaired mitophagy.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Interestingly, a combination of rotenone and Mdivi-1 induced a robust mitochondrial elongation, increased mitochondrial mass, and cellular senescence (Fig. 4A–D).”
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In the paper
“Rotenone resulted in increased mtROS (Supplemental Fig. S2K) and mitochondrial mass accumulation, as well as an increase in cellular senescence after 15 days of CSE treatment (Fig. 4A–D).”
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In the paper
“We found that nocodazole treatment inhibited perinuclear mitochondrial accumulation (Supplemental Fig. S1C, D) and decreased γ-H2AX foci formation after 24 hours in CSE-treated cells (Supplemental Fig. S1E) but caused cell death later (Supplemental Fig. S1F).”
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In the paper
“Furthermore, CSE treatment led to increased mtROS and decreased ATP levels in HFL1 cells with senescence (Fig. 1E, F).”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“CSE treatment for 15 days induced increased cytosolic p53 levels and its association with Parkin, which was reduced by nocodazole treatment (Supplemental Fig. S2E, F, H, I).”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Studies in the isolated mitochondria showed impaired Parkin translocation to mitochondria in CS-exposed mouse lungs, as well as in the lungs of human smokers and patients with COPD (Figs. 8E, F, and 9C, D).”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Furthermore, using Parkin overexpression in HFL1 cells, we observed a decrease in mitochondrial mass accumulation (Fig. 5G), but not much change in cellular senescence after 15 days of CSE treatment (Fig. 5H).”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Human COPD SAECs showed increased mitochondrial mass (Fig. 7A, B) and cellular senescence (Fig. 7C, D), which was further augmented by CSE treatment (Fig. 7A–D).”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“These results show that Parkin overexpression can restore mitochondrial mass accumulation but does not have a significant impact on cellular senescence when CS already establishes the cellular senescence.”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Parkin overexpression during CSE treatment restored mitophagy, as shown by recruitment of Parkin to mitochondria (Fig. 5A–C), which resulted in decreased perinuclear mitochondrial accumulation (Fig. 5D), and a slight decrease in γ-H2AX foci formation, but not much change in mtROS levels (Fig. 5E, F, and Supplemental Fig. S3A, B).”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This was associated with defective mitophagy and decreased mitochondrial function.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Furthermore, primary SAECs from patients with COPD exhibited increased cellular senescence and decreased mitophagy, which was further augmented by CSE treatment.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Although we have also observed increased mitochondrial fragmentation with high concentration of CSE treatment (data not shown), the objective of this study was to elucidate the role of mitochondrial quality control during cellular senescence (using low concentration of CSE treatment), which is one of the critical factors for COPD.”
plaindirect- 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.
None of the sources cited for this claim have been checked yet.
In the paper
“We have recently shown that CS leads to increased cellular senescence associated with increased reactive oxygen species (ROS) production in lung cells (3, 6, 8).”
What the sources say
- Not checked yetcites [3] Hwang J. W., Yao H., Caito S., Sundar I. K., Rahman I. (2013) Redox regulation of SIRT1 in inflammation and cellular senescence. Free Radic. Biol. Med. 61, 95–110 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [6] Yao H., Chung S., Hwang J. W., Rajendrasozhan S., Sundar I. K., Dean D. A., McBurney M. W., Guarente L., Gu W., Rönty M., Kinnula V. L., Rahman I. (2012) SIRT1 protects against emphysema via FOXO3-mediated reduction of premature senescence in mice. J. Clin. Invest. 122, 2032–2045 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [8] Yao H., Sundar I. K., Ahmad T., Lerner C., Gerloff J., Friedman A. E., Phipps R. P., Sime P. J., McBurney M. W., Guarente L., Rahman I. (2014) SIRT1 protects against cigarette smoke-induced lung oxidative stress via a FOXO3-dependent mechanism. Am. J. Physiol. Lung Cell. Mol. Physiol. 306, L816–L828 [DOI] [PMC free article] [PubMed] [Google Scholar] source
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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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Once recruited to mitochondria, Parkin mediates degradation of mitofusin-2 (Mfn2; a core protein involved in mitochondrial fusion) and hence prevents mitochondrial fusion.”
What the sources say
- Not checked yetcites [20] Yamano K., Fogel A. I., Wang C., van der Bliek A. M., Youle R. J. (2014) Mitochondrial Rab GAPs govern autophagosome biogenesis during mitophagy. eLife 3, e01612 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [21] Chen Y., Dorn G. W. II (2013) PINK1-phosphorylated mitofusin 2 is a Parkin receptor for culling damaged mitochondria. Science 340, 471–475 [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaindirect- 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. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Mitophagy is activated by mitochondrial membrane depolarization, followed by stabilization of a phosphatase and tensin homolog-induced putative kinase 1 (Pink1) on mitochondrial outer membrane, which then recruits an E3 ubiquitin ligase (Parkin) from the cytosol (17–19).”
What the sources say
- Not checked yetcites [17] Youle R. J., Narendra D. P. (2011) Mechanisms of mitophagy. Nat. Rev. Mol. Cell Biol. 12, 9–14 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [18] Bingol B., Tea J. S., Phu L., Reichelt M., Bakalarski C. E., Song Q., Foreman O., Kirkpatrick D. S., Sheng M. (2014) The mitochondrial deubiquitinase USP30 opposes parkin-mediated mitophagy. Nature 510, 370–375 [DOI] [PubMed] [Google Scholar] source
- Not checked yetcites [19] Vincow E. S., Merrihew G., Thomas R. E., Shulman N. J., Beyer R. P., MacCoss M. J., Pallanck L. J. (2013) The PINK1-Parkin pathway promotes both mitophagy and selective respiratory chain turnover in vivo. Proc. Natl. Acad. Sci. USA 110, 6400–6405 [DOI] [PMC free article] [PubMed] [Google Scholar] 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.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Cellular senescence is characterized by the activation of p16, p21, and p53, along with increased activity of senescence-associated β-galactosidase (SA-β-gal) (6, 7).”
What the sources say
- Not checked yetcites [6] Yao H., Chung S., Hwang J. W., Rajendrasozhan S., Sundar I. K., Dean D. A., McBurney M. W., Guarente L., Gu W., Rönty M., Kinnula V. L., Rahman I. (2012) SIRT1 protects against emphysema via FOXO3-mediated reduction of premature senescence in mice. J. Clin. Invest. 122, 2032–2045 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [7] Rodier F., Campisi J. (2011) Four faces of cellular senescence. J. Cell Biol. 192, 547–556 [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- 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. 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
“This suggests that mitochondrial structural changes or its dysfunction is induced by CS stress.”
hedgeddirect- 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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It may state two separate claims as one.
In the paper
“Mitochondrial fission highly correlates with cell apoptosis and mitophagy (selective degradation of damaged mitochondria), whereas mitochondrial fusion has the opposite role (13).”
What the sources say
- Not checked yetcites [13] Youle R. J., van der Bliek A. M. (2012) Mitochondrial fission, fusion, and stress. Science 337, 1062–1065 [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- 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. It may state two separate claims as one.
In the paper
“Similarly, elongated mitochondria with increased mitochondrial fusion activity occur during long-term CSE treatment in a human lung epithelial cell line (15).”
What the sources say
- Not checked yetcites [15] Hoffmann R. F., Zarrintan S., Brandenburg S. M., Kol A., de Bruin H. G., Jafari S., Dijk F., Kalicharan D., Kelders M., Gosker H. R., Ten Hacken N. H., van der Want J. J., van Oosterhout A. J., Heijink I. H. (2013) Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells. Respir. Res. 14, 97 [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaincorrelational- 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.
In the paper
“Cigarette smoke extract (CSE) induces mitochondrial fission in human smooth muscle cells, which may contribute to cell death during the pathogenesis of COPD/emphysema (14).”
What the sources say
- Not checked yetcites [14] Aravamudan B., Kiel A., Freeman M., Delmotte P., Thompson M., Vassallo R., Sieck G. C., Pabelick C. M., Prakash Y. S. (2014) Cigarette smoke-induced mitochondrial fragmentation and dysfunction in human airway smooth muscle. Am. J. Physiol. Lung Cell. Mol. Physiol. 306, L840–L854 [DOI] [PMC free article] [PubMed] [Google Scholar] source
hedgedconditional- 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.
Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Damaged or dysfunctional mitochondria are cleared from the cells by a process called mitophagy (16–18).”
What the sources say
- Not checked yetcites [16] Ashrafi G., Schwarz T. L. (2013) The pathways of mitophagy for quality control and clearance of mitochondria. Cell Death Differ. 20, 31–42 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [17] Youle R. J., Narendra D. P. (2011) Mechanisms of mitophagy. Nat. Rev. Mol. Cell Biol. 12, 9–14 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [18] Bingol B., Tea J. S., Phu L., Reichelt M., Bakalarski C. E., Song Q., Foreman O., Kirkpatrick D. S., Sheng M. (2014) The mitochondrial deubiquitinase USP30 opposes parkin-mediated mitophagy. Nature 510, 370–375 [DOI] [PubMed] [Google Scholar] 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.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“These autophagosomes containing the damaged mitochondria fuse with lysosomes which are cleared from the cells (16–21).”
What the sources say
- Not checked yetcites [16] Ashrafi G., Schwarz T. L. (2013) The pathways of mitophagy for quality control and clearance of mitochondria. Cell Death Differ. 20, 31–42 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [17] Youle R. J., Narendra D. P. (2011) Mechanisms of mitophagy. Nat. Rev. Mol. Cell Biol. 12, 9–14 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [18] Bingol B., Tea J. S., Phu L., Reichelt M., Bakalarski C. E., Song Q., Foreman O., Kirkpatrick D. S., Sheng M. (2014) The mitochondrial deubiquitinase USP30 opposes parkin-mediated mitophagy. Nature 510, 370–375 [DOI] [PubMed] [Google Scholar] source
- Not checked yetcites [19] Vincow E. S., Merrihew G., Thomas R. E., Shulman N. J., Beyer R. P., MacCoss M. J., Pallanck L. J. (2013) The PINK1-Parkin pathway promotes both mitophagy and selective respiratory chain turnover in vivo. Proc. Natl. Acad. Sci. USA 110, 6400–6405 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [20] Yamano K., Fogel A. I., Wang C., van der Bliek A. M., Youle R. J. (2014) Mitochondrial Rab GAPs govern autophagosome biogenesis during mitophagy. eLife 3, e01612 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [21] Chen Y., Dorn G. W. II (2013) PINK1-phosphorylated mitofusin 2 is a Parkin receptor for culling damaged mitochondria. Science 340, 471–475 [DOI] [PMC free article] [PubMed] [Google Scholar] 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.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“This initiates the localization of damaged mitochondria to membranes containing microtubule-associated protein light-chain 3 (LC3) leading to the formation of autophagosomes (20, 21).”
What the sources say
- Not checked yetcites [20] Yamano K., Fogel A. I., Wang C., van der Bliek A. M., Youle R. J. (2014) Mitochondrial Rab GAPs govern autophagosome biogenesis during mitophagy. eLife 3, e01612 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [21] Chen Y., Dorn G. W. II (2013) PINK1-phosphorylated mitofusin 2 is a Parkin receptor for culling damaged mitochondria. Science 340, 471–475 [DOI] [PMC free article] [PubMed] [Google Scholar] 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.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. 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
“Furthermore, during earlier time points, CSE stress results in increased perinuclear mitochondrial clustering, which may be the mechanism whereby dysfunctional mitochondria trigger the cellular senescence process.”
hedgedconditional- 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
“Overall, CS impairs mitophagy, which is associated with reduced Parkin mitochondrial translocation via p53.”
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
“Accumulation of damaged or dysfunctional mitochondria, due to impaired mitophagy, has been associated with many pathologic conditions (22–24).”
What the sources say
- Not checked yetcites [22] Osellame L. D., Duchen M. R. (2013) Defective quality control mechanisms and accumulation of damaged mitochondria link Gaucher and Parkinson diseases. Autophagy 9, 1633–1635 [DOI] [PubMed] [Google Scholar] source
- Not checked yetcites [23] Heeman B., Van den Haute C., Aelvoet S. A., Valsecchi F., Rodenburg R. J., Reumers V., Debyser Z., Callewaert G., Koopman W. J., Willems P. H., Baekelandt V. (2011) Depletion of PINK1 affects mitochondrial metabolism, calcium homeostasis and energy maintenance. J. Cell Sci. 124, 1115–1125 [DOI] [PubMed] [Google Scholar] source
- Not checked yetcites [24] Fang E. F., Scheibye-Knudsen M., Brace L. E., Kassahun H., SenGupta T., Nilsen H., Mitchell J. R., Croteau D. L., Bohr V. A. (2014) Defective mitophagy in XPA via PARP-1 hyperactivation and NAD(+)/SIRT1 reduction. Cell 157, 882–896 [DOI] [PMC free article] [PubMed] [Google Scholar] source
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.
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
“From these results, we infer that CSE treatments lead to mitochondrial dysfunction, and mitochondria become highly interconnected and accumulated in senescent cells.”
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.
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
“These results show that restoring mitophagy and attenuating mtROS can prevent the progression of cellular senescence in primary lung fibroblasts.”
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.
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
“These results provide evidence that mitophagy is highly impaired during CS exposure in mouse lungs as well as in the lungs of smokers and patients with COPD, which may be a contributing factor for cellular senescence during the pathogenesis of COPD.”
boostedcorrelational- 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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Mito-Tempo (MitoT) was used at different concentrations (100 nM, 500 nM, 1 µM, and 2 µM), and a dose (1 µM) that induced substantial reduction in mitochondrial reactive oxygen species (mtROS) was used for further experiments.”
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.
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
“We have shown here a previously unknown molecular pathway for CS stress-induced cellular senescence via mitochondrial dysfunction in vitro in human lung fibroblasts and human primary SAECs, and in vivo in mouse lungs as well as ex vivo in the lungs of patients with COPD.”
boosteddirect- 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.
In the paper
“We have also previously shown that human COPD and smoker lungs are associated with increased p16 and p21 levels, as well as SA-β-gal activity (6).”
What the sources say
- Not checked yetcites [6] Yao H., Chung S., Hwang J. W., Rajendrasozhan S., Sundar I. K., Dean D. A., McBurney M. W., Guarente L., Gu W., Rönty M., Kinnula V. L., Rahman I. (2012) SIRT1 protects against emphysema via FOXO3-mediated reduction of premature senescence in mice. J. Clin. Invest. 122, 2032–2045 [DOI] [PMC free article] [PubMed] [Google Scholar] source
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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The dose of CSE was chosen on the basis of dose response curve generated, which induced substantial cellular senescence with minimal apoptosis for a period of 10 or 15 days with alternate days of CSE treatment.”
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.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Parkin overexpression is shown to delay aging in flies (47, 48).”
What the sources say
- Not checked yetcites [47] Ballweg K., Mutze K., Königshoff M., Eickelberg O., Meiners S. (2014) Cigarette smoke extract affects mitochondrial function in alveolar epithelial cells. Am. J. Physiol. Lung Cell. Mol. Physiol. 307, L895–L907 [DOI] [PubMed] [Google Scholar] source
- Not checked yetcites [48] Hara H., Araya J., Ito S., Kobayashi K., Takasaka N., Yoshii Y., Wakui H., Kojima J., Shimizu K., Numata T., Kawaishi M., Kamiya N., Odaka M., Morikawa T., Kaneko Y., Nakayama K., Kuwano K. (2013) Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence. Am. J. Physiol. Lung Cell. Mol. Physiol. 305, L737–L746 [DOI] [PubMed] [Google Scholar] source
plaindirect- 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
“Parkin overexpression has been shown to increase the life span in flies and reduces oxidative stress by activating mitophagy (50, 51).”
What the sources say
- Not checked yetcites [50] Rana A., Rera M., Walker D. W. (2013) Parkin overexpression during aging reduces proteotoxicity, alters mitochondrial dynamics, and extends lifespan. Proc. Natl. Acad. Sci. USA 110, 8638–8643 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [51] Saini N., Georgiev O., Schaffner W. (2011) The parkin mutant phenotype in the fly is largely rescued by metal-responsive transcription factor (MTF-1). Mol. Cell. Biol. 31, 2151–2161 [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaindirect- 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. It may state two separate claims as one.
In the paper
“A recent study has shown that increased p53 cytosolic localization prevents Parkin translocation to mitochondria during organismal aging (27).”
What the sources say
- Not checked yetcites [27] Hoshino A., Mita Y., Okawa Y., Ariyoshi M., Iwai-Kanai E., Ueyama T., Ikeda K., Ogata T., Matoba S. (2013) Cytosolic p53 inhibits Parkin-mediated mitophagy and promotes mitochondrial dysfunction in the mouse heart. Nat. Commun. 4, 2308 [DOI] [PubMed] [Google Scholar] 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.
- Based: passes — The paper gives a reason why it holds.
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
“Therefore, CS causes mitophagy impairment and mtROS generation, which may drive DNA damage and cellular senescence.”
hedgedconditional- 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
“mtROS has been shown as a key inducer for premature aging, and mtROS inhibitor reduces senescence in bone marrow mesenchymal stem cells (52, 53).”
What the sources say
- Not checked yetcites [52] Wu J., Niu J., Li X., Wang X., Guo Z., Zhang F. (2014) TGF-β1 induces senescence of bone marrow mesenchymal stem cells via increase of mitochondrial ROS production. BMC Dev. Biol. 14, 21 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [53] Tao R., Vassilopoulos A., Parisiadou L., Yan Y., Gius D. (2014) Regulation of MnSOD enzymatic activity by Sirt3 connects the mitochondrial acetylome signaling networks to aging and carcinogenesis. Antioxid. Redox Signal. 20, 1646–1654 [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaindirect- 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.
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
“This indicates that cytosolic translocation of p53 was partly mediated by perinuclear mitochondrial accumulation, followed by DNA damage foci formation.”
hedgedconditional- 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
“It is interesting to note that MitoT treatment alone did not show any significant effect on cellular senescence, which may be due to its insufficient concentration and duration used.”
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.
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
“Altogether, both mitophagy impairment and mtROS generation contribute to CS-induced cellular senescence.”
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
“Both Pink1 and Parkin knockout mice exhibit increased ROS levels and mitochondrial dysfunction (43, 44), and persistent increased ROS is one of the important factors in accelerating cellular senescence (42, 45).”
What the sources say
- Not checked yetcites [43] Palacino J. J., Sagi D., Goldberg M. S., Krauss S., Motz C., Wacker M., Klose J., Shen J. (2004) Mitochondrial dysfunction and oxidative damage in parkin-deficient mice. J. Biol. Chem. 279, 18614–18622 [DOI] [PubMed] [Google Scholar] source
- Not checked yetcites [44] Haque M. E., Mount M. P., Safarpour F., Abdel-Messih E., Callaghan S., Mazerolle C., Kitada T., Slack R. S., Wallace V., Shen J., Anisman H., Park D. S. (2012) Inactivation of Pink1 gene in vivo sensitizes dopamine-producing neurons to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and can be rescued by autosomal recessive Parkinson disease genes, Parkin or DJ-1. J. Biol. Chem. 287, 23162–23170 [DOI] [PMC free article] [PubMed] [Google Scholar] 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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Although long-term nocodazole treatment led to cell death, we were therefore unable to directly evaluate the effect of perinuclear mitochondrial accumulation on cellular senescence.”
plaindirect- 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.
- 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
“Parkin is a core mitophagy-regulating protein, which is recruited to damaged or depolarized mitochondria to induce mitochondrial clearance (16–19).”
What the sources say
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plaindirect- 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.
In the paper
“A recent study has shown increased mitophagy with acute CSE treatment in cultured lung epithelial cells, whereas mitochondria were highly fragmented in CS-exposed mouse lung epithelial cells (55).”
What the sources say
- Not checked yetcites [55] Mizumura K., Cloonan S. M., Nakahira K., Bhashyam A. R., Cervo M., Kitada T., Glass K., Owen C. A., Mahmood A., Washko G. R., Hashimoto S., Ryter S. W., Choi A. M. (2014) Mitophagy-dependent necroptosis contributes to the pathogenesis of COPD. J. Clin. Invest. 124, 3987–4003 [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaincorrelational- 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
“A recent study has shown increased mitophagy with acute CSE treatment in cultured lung epithelial cells, whereas mitochondria were highly fragmented in CS-exposed mouse lung epithelial cells (55).”
What the sources say
- Not checked yetcites [55] Mizumura K., Cloonan S. M., Nakahira K., Bhashyam A. R., Cervo M., Kitada T., Glass K., Owen C. A., Mahmood A., Washko G. R., Hashimoto S., Ryter S. W., Choi A. M. (2014) Mitophagy-dependent necroptosis contributes to the pathogenesis of COPD. J. Clin. Invest. 124, 3987–4003 [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaindirect- 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.
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
“In summary, we show here for the first time that the mechanisms of defective mitophagy lead to accumulation of dysfunctional and damaged mitochondria and, hence, augmented cellular senescence during CS exposure in vitro in lung epithelial cells and fibroblasts, mouse lungs, as well as human smokers and patients with COPD (Fig. 10).”
boosteddirect- 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
“This is associated with a reduction of Parkin-mediated mitophagy and an increase in mtROS-induced DNA damage.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
In the paper
“There is a study showing elongated mitochondria with increased mitochondrial fusion activity during long-term CSE treatment in a human lung epithelial cell line (15), which is in agreement with our findings.”
What the sources say
- Not checked yetcites [15] Hoffmann R. F., Zarrintan S., Brandenburg S. M., Kol A., de Bruin H. G., Jafari S., Dijk F., Kalicharan D., Kelders M., Gosker H. R., Ten Hacken N. H., van der Want J. J., van Oosterhout A. J., Heijink I. H. (2013) Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells. Respir. Res. 14, 97 [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaindirect- 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.
None of the sources cited for this claim have been checked yet.
In the paper
“The discrepancies among these studies may be due to different cell culture conditions and the concentration and duration of CSE used (14, 15, 48).”
What the sources say
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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
“Pink1 deficiency leads to mitochondrial damage and hence promotes lung fibrosis (56), whereas a decreased expression of mitochondrial fission proteins Drp1 and mitochondrial fission 1 protein induces cellular senescence via a Pink1-dependent manner (57).”
What the sources say
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plaindirect- 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
“Pink1 deficiency leads to mitochondrial damage and hence promotes lung fibrosis (56), whereas a decreased expression of mitochondrial fission proteins Drp1 and mitochondrial fission 1 protein induces cellular senescence via a Pink1-dependent manner (57).”
What the sources say
- Not checked yetcites [56] Bueno M., Lai Y. C., Romero Y., Brands J., St Croix C. M., Kamga C., Corey C., Herazo-Maya J. D., Sembrat J., Lee J. S., Duncan S. R., Rojas M., Shiva S., Chu C. T., Mora A. L. (2015) PINK1 deficiency impairs mitochondrial homeostasis and promotes lung fibrosis. J. Clin. Invest. 125, 521–538 [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaindirect- 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. 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
“Overall, these findings unravel new insights into the molecular mechanisms of mitophagy regulating cellular senescence during CS stress-induced lung pathophysiologic responses.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
None of the sources cited for this claim have been checked yet.
In the paper
“Recent studies have also shown that smooth muscle and transformed lung epithelial cells are equally sensitive to CS-induced cellular senescence (14, 15).”
What the sources say
- Not checked yetcites [14] Aravamudan B., Kiel A., Freeman M., Delmotte P., Thompson M., Vassallo R., Sieck G. C., Pabelick C. M., Prakash Y. S. (2014) Cigarette smoke-induced mitochondrial fragmentation and dysfunction in human airway smooth muscle. Am. J. Physiol. Lung Cell. Mol. Physiol. 306, L840–L854 [DOI] [PMC free article] [PubMed] [Google Scholar] source
- Not checked yetcites [15] Hoffmann R. F., Zarrintan S., Brandenburg S. M., Kol A., de Bruin H. G., Jafari S., Dijk F., Kalicharan D., Kelders M., Gosker H. R., Ten Hacken N. H., van der Want J. J., van Oosterhout A. J., Heijink I. H. (2013) Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells. Respir. Res. 14, 97 [DOI] [PMC free article] [PubMed] [Google Scholar] source
plain- 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.
The paper relies on this without support.
The molecular mechanism by which cigarette smoke induces cellular senescence is unknown.
“However, the molecular mechanism by which CS induces cellular senescence is unknown.”
The paper relies on this without support.
It is not clear whether cigarette smoke stress-induced lung cellular senescence is due to mitochondrial dysfunction via defective mitophagy.
“However, it is not clear whether CS stress-induced lung cellular senescence is due to mitochondrial dysfunction via defective mitophagy.”
The paper relies on this without support.
The molecular mechanism underlying cigarette smoke-induced mitochondrial structural changes or dysfunction and their impact during cellular senescence is not known.
“However, the molecular mechanism underlying these phenomena and their impact during cellular senescence is not known.”
The paper relies on this without support.
Most cellular reactive oxygen species are predominantly generated by mitochondria.
“Most of the cellular ROS are predominantly generated by mitochondria”
The paper relies on this without support.
The mechanisms and signaling pathways associated with CS stress-induced cellular senescence and COPD are not known.
“Although a well-appreciated phenomenon, the mechanisms and the signaling pathways associated with CS stress-induced cellular senescence and COPD per se are not known.”
The paper relies on this without support.
One of the major contributing factors of CS-induced COPD is oxidative stress.
“One of the major contributing factors of CS-induced COPD is oxidative stress.”
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
“Nonetheless, the inhibition of mitophagy associated with the genetic deletion of Prkn worsen the effect of CS, as it promotes the entry of epithelial alveolar cells in the senescent state (Ahmad et al, 2015).”
From Autophagy in major human diseases (2021) · cites this paper as Ahmad et al, 2015
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ MATERIALS AND METHODS
“Cells were treated with different concentrations of Mdivi-1 (1–10 μM, catalog number M0199; Sigma-Aldrich, St. Louis, MO, USA) or bafilomycin (10 nM, catalog number B1793; Sigma-Aldrich) for 15 days”
§ MATERIALS AND METHODS
“whereas bafilomycin was used for 10 days with alternate day treatments.”
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Metadata
- Authors
- Ahmad, T., Sundar, I. K., Lerner, C. A., Gerloff, J., Tormos, A. M., Yao, H., & Rahman, I.
- Affiliations
- University of Rochester Medicine (US)
- Corresponding author
- Yao, Hongwei
- Rahman, Irfan
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2015-03-19
- Volume
- 29
- Issue
- 7
- Pages
- 2912-2929
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- PMC
- PMC4478793
- OpenAlex
- W2169986172
- Semantic Scholar
- 5b955ac0453445e460563db134eebe8e6445cc9b
- Cited by
- 264
- References
- 60
- Citations by year
- 2026: 13 · 2025: 17 · 2024: 17 · 2023: 33 · 2022: 30 · 2021: 35 · 2020: 25 · 2019: 22 · 2018: 25 · 2017: 25 · 2016: 16 · 2015: 6
- FWCI
- 18.74
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The FASEB Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (P30‐ES01247)
- National Heart, Lung, and Blood Institute (2R01HL085613, 1R01HL092842)
- American Lung Association (RG‐266456‐N, RG‐305393)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Keywords
- cigarette smoke, cellular senescence, mitophagy, chronic obstructive pulmonary disease, Parkin, p53, mitochondrial damage, small airway epithelial cells, lung fibroblasts, emphysema, MitoTEMPO, subcellular signaling, mitochondrial quality control
- MeSH terms
- Animals, Antioxidants, Cells, Cultured, DNA Damage, Fibroblasts, Humans, Lung, Mice, Inbred C57BL, Organophosphorus Compounds, Piperidines, Smoking, Case-Control Studies, Cellular Senescence, Reactive Oxygen Species, Respiratory Mucosa, Pulmonary Disease, Chronic Obstructive, Ubiquitin-Protein Ligases, Mice, Mitophagy
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