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Cited by 61Muscle Physiology and DisordersNutrition and Health in AgingMuscle metabolism and nutrition

Nutraceuticals in the Prevention and Treatment of the Muscle Atrophy

Open access
Wang, Yanan, Liu, Qing, Quan, Helong, Kang, Seong-Gook, Huang, Kunlun, Tong, Tao·2021·Nutrients
DOI 10.3390/nu13061914PMC PMC8227811
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Abstract

Imbalance of protein homeostasis, with excessive protein degradation compared with protein synthesis, leads to the development of muscle atrophy resulting in a decrease in muscle mass and consequent muscle weakness and disability. Potential triggers of muscle atrophy include inflammation, malnutrition, aging, cancer, and an unhealthy lifestyle such as sedentariness and high fat diet. Nutraceuticals with preventive and therapeutic effects against muscle atrophy have recently received increasing attention since they are potentially more suitable for long-term use. The implementation of nutraceutical intervention might aid in the development and design of precision medicine strategies to reduce the burden of muscle atrophy. In this review, we will summarize the current knowledge on the importance of nutraceuticals in the prevention of skeletal muscle mass loss and recovery of muscle function. We also highlight the cellular and molecular mechanisms of these nutraceuticals and their possible pharmacological use, which is of great importance for the prevention and treatment of muscle atrophy.

AI snapshot

Written from the paper’s full text.

TL;DR

This review summarizes preclinical evidence that dietary nutrients, phytochemicals, and probiotics can prevent or attenuate skeletal muscle atrophy mainly by suppressing MAFbx/MuRF1, inflammation, oxidative stress, and myostatin while activating IGF-1/PI3K/Akt/mTOR signaling. It concludes that clinical evidence and structure-function data remain insufficient for marketed nutraceutical therapies.

Key findings

  • Protein, amino acid, and peptide interventions—including whey protein, leucine, branched-chain amino acids, glutamine, taurine, creatine, S-allyl cysteine, and soybean-derived peptides—increase muscle mass/strength or reduce atrophy markers in various in vitro and in vivo models, often via mTOR/PI3K/Akt activation and downregulation of MAFbx/MuRF1.
  • Minerals, vitamins, and fatty acids show preventive effects: daily calcium intake was significantly lower in subjects with sarcopenia (2.7%) than without (6.3%) in older non-obese Korean adults; the Maastricht sarcopenia study reported 10–18% lower intake of certain nutrients such as magnesium; 12-week magnesium supplementation may improve or delay age-related decline in muscle physical performance and strength in healthy elderly women; and 500 mg/kg/day nicotinamide mononucleotide for 7 days reversed muscle atrophy in aged C57BL/6J mice by decreasing MAFbx and MuRF1.
  • Phytochemicals—polyphenols, flavonoids, polysaccharides, alkaloids, and triterpenoids—reduce atrophy-related genes and promote myogenesis; examples include 12 weeks of vitamin C supplementation restoring vitamin C deficiency-induced muscle atrophy in mice, 4 weeks of oral fucoidan improving extensor digitorum longus and soleus fiber cross-sectional area in C57BL/6 mice, and 14 days of ampelopsin attenuating dexamethasone-induced muscle atrophy in SD rats.
  • Probiotics and gut microbiota are implicated: Lactobacillus supplementation reduced MAFbx/MuRF1 and inflammatory cytokines in leukemia BALB/c mice; 13-week intake of inulin and fructooligosaccharides complex increased grip strength in elderly people over 65 years old; and germ-free mice showed upregulated MAFbx and MuRF-1, which was reduced after transplanting gut microbiota from pathogen-free mice.

Methods

  • Narrative review; research articles on nutraceutical intervention for muscle atrophy and mechanisms of muscle atrophy were collected using PubMed, Web of Science, Scopus, Google Scholar, Springer, and Wiley, with keywords such as muscle atrophy, protein synthesis/degradation, molecular mechanisms, nutraceutical, nutrient, oxidative stress, muscle mass, muscle strength, microbiota, glucocorticoid, and phytochemical.
  • Identified articles and relevant citations within them were reviewed; no systematic review registration, search dates, inclusion/exclusion criteria, or quality assessment are reported in the text.
  • Evidence is synthesized descriptively in tables by nutrient/phytochemical class and model; no meta-analysis is reported.

Limitations

  • The paper states that most nutraceuticals have been examined only in preclinical trials, either in vitro or in vivo; clinical evidence is not sufficient and is urgently needed, little evidence supports the structure-function relationship of phytochemicals in skeletal muscle atrophy, and probiotic mechanisms are unclear and lacking.
  • The paper calls for future clinical trials to examine anti-muscle atrophy action and dose, studies of bioavailability and whole-body metabolism, use of 3D cell models, organoid models, in silico high-throughput screening, and nutrigenomics.
  • Evident from the text: as a narrative review without a systematic protocol or quantitative synthesis, it combines heterogeneous models, inducers, species, and outcome measures, making direct comparisons across studies difficult.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.3390/nu13061914

Cites

168 of 168 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 207 cited sources checked · 0 supported · 0 flagged

  • Premisecitation

    Activation of IGF-1/PI3K/Akt signaling represses MAFbx and MuRF1 gene expression via decreasing FoxO expression and activity.

    “On the contrary, the activation of insulin-like growth factor (IGF-1)/phosphoinositide 3-kinase (PI3K)/Akt signaling pathway represses the MAFbx and MuRF1 gene expression via decreasing the expression and activity of FoxO.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [5] Ebert, 2019, Skeletal Muscle Atrophy: Discovery of Mechanisms and Potential Therapies, Physiology source

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  • Premisecitation

    Muscle atrophy is caused by excessive protein degradation relative to protein synthesis.

    “Muscle atrophy is a worldwide chronic progressive muscle disease due to excessive protein degradation versus protein synthesis.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [1] Cohen, 2015, Muscle Wasting in Disease: Molecular Mechanisms and Promising Therapies, Nat. Rev. Drug Discov. source

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  • Premisecitation

    Various stimuli including aging, genetics, denervation, starvation, unhealthy lifestyle, systemic pathologies, and long-term drug therapy further skeletal muscle loss and weakness.

    “Various stimuli, such as aging, genetics, denervation, starvation, unhealthy lifestyle (i.e., sedentariness, high fat diet (HFD)), systemic pathologies (i.e., diabetes, inflammation, cancer), and long-term drug therapy (i.e., glucocorticoids) are known to further skeletal muscle loss and weakness [2,3,4].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [2] Mirzoev, T.M. (2020). Skeletal Muscle Recovery from Disuse Atrophy: Protein Turnover Signaling Andstrategies for Accelerating Muscle Regrowth. Int. J. Mol. Sci., 21. source

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    • cites [3] Jackman, 2004, The Molecular Basis of Skeletal Muscle Atrophy, Am. J. Physiol. Cell Physiol. source

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    • cites [4] Sartori, 2021, Mechanisms of Muscle Atrophy and Hypertrophy: Implications in Health and Disease, Nat. Commun. source

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  • Premisecitation

    Under starvation, muscle disuse, glucocorticoid excess, and aging, glucocorticoid receptor and FoxO increase MuRF1 expression and promote muscle atrophy.

    “Under a wide range of conditions including starvation, muscle disuse, glucocorticoid excess, and aging, the glucocorticoid receptor and transcription factor forkhead box O (FoxO) increase the expression of MuRF1 and promote muscle atrophy [5].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [5] Ebert, 2019, Skeletal Muscle Atrophy: Discovery of Mechanisms and Potential Therapies, Physiology source

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  • Premisecitation

    Oxidative stress is a major trigger of imbalance between protein synthesis and degradation leading to muscle atrophy.

    “Oxidative stress, characterized by increased reactive oxygen species (ROS) production and impairment of antioxidant defense systems, is also a major trigger of imbalance between protein synthesis and degradation leading to muscle atrophy [10,11].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [10] Moylan, 2007, Oxidative Stress, Chronic Disease, and Muscle Wasting, Muscle Nerve source

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    • cites [11] Zuo, 2015, Redox Characterization of Functioning Skeletal Muscle, Front. Physiol. source

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    Premisecitation

    Mechanisms underlying HFD-induced atrophy are not fully understood, but recent experimental data suggest elevated toxic lipid metabolites and pro-inflammatory cytokines may contribute to decreased muscle mass and strength.

    “For example, the mechanisms underlying HFD-induced atrophy are not fully understood, but recent experimental data suggest that multiple factors such as elevated levels of toxic lipid metabolites and pro-inflammatory cytokines may contribute to a decrease in muscle mass and strength [14].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [14] Sun, 2020, Amyotrophy Induced by a High-Fat Diet Is Closely Related to Inflammation and Protein Degradation Determined by Quantitative Phosphoproteomic Analysis in Skeletal Muscle of C57BL/6 J Mice, J. Nutr. source

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    • Rests on an assumption: The mechanisms inducing muscle atrophy between the numerous models presented are not identical.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    TNF-α, IL-6, and IL-1 have long been considered mediators of cancer-induced muscle atrophy.

    “The pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukine-6 (IL-6), and interleukine-1 (IL-1), have long been considered as mediators of cancer-induced muscle atrophy [1].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [1] Cohen, 2015, Muscle Wasting in Disease: Molecular Mechanisms and Promising Therapies, Nat. Rev. Drug Discov. source

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    Premisecitation

    Activation of IGF-1/PI3K/Akt pathway stimulates protein synthesis and induces muscle growth via mTOR kinase.

    “In addition to inhibiting muscle atrophy, the activation of insulin-like growth factor 1 (IGF-1)/PI3K/Akt pathway also stimulates protein synthesis and induces muscle growth via rapamycin complex (mTOR) kinase [5].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [5] Ebert, 2019, Skeletal Muscle Atrophy: Discovery of Mechanisms and Potential Therapies, Physiology source

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    Premisenone given

    Myostatin induces muscle fiber atrophy by activating Smad2 and Smad3 and suppresses protein synthesis by inhibiting Akt.

    “Myostatin, a member of the transforming growth factor-β (TGF-β) superfamily and critical autocrine inhibitor of skeletal muscle growth, induces muscle fiber atrophy by the activation of Smad2 and Smad3 and suppresses protein synthesis by the inhibition of protein kinase B (Akt) (Figure 1).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Muscle atrophy is characterized by muscle mass loss, muscle weakness, and disability, which are associated with impaired quality of life.

    “It is characterized by muscle mass loss, muscle weakness, and disability, all of which are associated with an impaired quality of life [1].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [1] Cohen, 2015, Muscle Wasting in Disease: Molecular Mechanisms and Promising Therapies, Nat. Rev. Drug Discov. source

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    Premisecitation

    Enhanced generation of mitochondrial ROS may be a common factor in denervation-induced atrophy.

    “Enhanced generation of mitochondrial ROS may be a common factor in the mechanism underlying denervation-induced atrophy [15].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [15] Muller, 2007, Denervation-Induced Skeletal Muscle Atrophy Is Associated with Increased Mitochondrial Ros Production, Am. J. Physiol. Regul. Integr. Comp. Physiol. source

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    Premisecitation

    Mice deficient in either MAFbx or MuRF1 are resistant to atrophy.

    “Mice deficient in either MAFbx or MuRF1 were demonstrated to be resistant to atrophy [7].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [7] Bodine, 2001, Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy, Science source

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    Premisecitation

    Gut microbiota has been proposed as an environmental factor involved in regulation of host immunity and muscle metabolism.

    “Recently, gut microbiota has been proposed as an environmental factor involved in the regulation of host immunity and muscle metabolism [12,13].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [12] Bindels, 2013, Muscle Wasting: The Gut Microbiota as a New Therapeutic Target?, Int. J. Biochem. Cell Biol. source

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    • cites [13] Ticinesi, A., Lauretani, F., Milani, C., Nouvenne, A., Tana, C., Del Rio, D., Maggio, M., Ventura, M., and Meschi, T. (2017). Aging Gut Microbiota at the Cross-Road between Nutrition, Physical Frailty, and Sarcopenia: Is There a Gut-Muscle Axis?. Nutrients, 9. source

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    Premisecitation

    l-glutamine improves C2C12 cell differentiation and prevents TNF-α-induced myotube atrophy via reducing p38 MAPK signal transduction.

    “l-glutamine improves C2C12 cells differentiation and prevents TNF-α-induced myotube atrophy via reducing p38 mitogen-activated protein kinase (MAPK) signal transduction [35].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [35] Girven, 2016, L-Glutamine Improves Skeletal Muscle Cell Differentiation and Prevents Myotube Atrophy after Cytokine (TNF-α) Stress Via Reduced p38 MAPK Signal Transduction, J. Cell. Physiol. source

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    Premisecitation

    Evidence from preclinical studies reveals nutraceuticals play a significant role in maintaining muscle health and are potential therapeutic agents in a broad range of muscle atrophy models.

    “Evidence from various preclinical studies has revealed that nutraceuticals play a significant role in maintaining muscle health and emerge as potential therapeutic agents in a broad range of muscle atrophy models [17,18].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [17] Kim, 2020, Flavonoids: Nutraceutical Potential for Counteracting Muscle Atrophy, Food Sci. Biotechnol. source

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    • cites [18] Salucci, 2020, Polyphenols and Their Potential Role in Preventing Skeletal Muscle Atrophy, Nutr. Res. source

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    • Rests on an assumption: Nutraceuticals are potentially more suitable for long-term use than traditional therapeutic agents.

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    Premisecitation

    Soluble whey protein hydrolysate increases grip strength, muscle mass, and cross-sectional area of muscle fiber and ameliorates immobilization-induced C57BL/6 mice muscle atrophy via regulating PI3K/Akt pathway.

    “Shin et al. reported that soluble whey protein hydrolysate increases grip strength, muscle mass, and cross-sectional area of muscle fiber and meliorates immobilization-induced C57BL/6 mice muscle atrophy via regulating the PI3K/Akt pathway [21].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [21] Shin, J.E., Park, S.J., Ahn, S.I., and Choung, S.Y. (2020). Soluble Whey Protein Hydrolysate Ameliorates Muscle Atrophy Induced by Immobilization via Regulating the PI3K/Akt Pathway in C57BL/6 Mice. Nutrients, 12. source

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    Premisecitation

    In cachexia-inducing tumor NMRI mice, leucine or valine increase protein synthesis and attenuate increased protein degradation.

    “In cachexia-inducing tumor Naval Medical Research Institute mice with a significant suppression in the loss of body weight, leucine or valine could increase protein synthesis and attenuate the increased protein degradation [26].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [26] Eley, 2007, Effect of Branched-Chain Amino Acids on Muscle Atrophy in Cancer Cachexia, Biochem. J. source

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    Premisecitation

    Isoleucine acts as an intermediate to drive muscle protein synthesis and reduce the rate of protein breakdown.

    “Similar to leucine and valine, isoleucine acts as an intermediate to drive muscle protein synthesis and reduce the rate of protein breakdown [27].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [27] Appuhamy, 2012, Isoleucine and Leucine Independently Regulate mTOR Signaling and Protein Synthesis in MAC-T Cells and Bovine Mammary Tissue Slices, J. Nutr. source

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    Premisecitation

    Amino acid complex supplementation ameliorates angiotensin II-induced muscle atrophy and increases skeletal muscle weight and gastrocnemius tissue cross-sectional area.

    “The supplementation of amino acid complex (leucine: isoleucine: valine = 2:1:1; 3% in tap water) ameliorates angiotensin II-induced muscle atrophy and increases skeletal muscle weight and gastrocnemius tissue cross-sectional area [29].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [29] Yamanashi, 2020, Branched-Chain Amino Acid Supplementation Ameliorates Angiotensin II-Induced Skeletal Muscle Atrophy, Life Sci. source

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    Premisecitation

    Oral administration of a high protein liquid nutritional supplement (milk protein, whey protein, leucine, and citrulline) inhibits intermittent loading-induced muscle atrophy and increases muscle mass by activating mTORC1 signaling.

    “Oral administration of a high protein liquid nutritional supplement (milk protein, whey protein, leucine, and citrulline) inhibits intermittent loading-induced muscle atrophy and increases muscle mass by activating the mTORC1 signaling pathway (Ribosomal protein S6 kinase (p70S6K) and ribosomal protein S6 (rpS6)) [20].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [20] Miyatake, S., Hino, K., Natsui, Y., Ebisu, G., and Fujita, S. (2020). Protein supplementation enhances the Protein Supplementation Enhances the Effects of Intermittent Loading on Skeletal Muscles by Activating the mTOR Signaling Pathway in a Rat Model of Disuse Atrophy. Nutrients, 12. source

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    Premisecitation

    Leucine supplementation can offset anabolic resistance and increases muscle protein synthesis in old women.

    “In addition, supplementation of leucine can offset anabolic resistance and increases muscle protein synthesis in old women [24].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [24] Wilkinson, 2018, Effects of Leucine-Enriched Essential Amino Acid and Whey Protein Bolus Dosing Upon Skeletal Muscle Protein Synthesis at Rest and after Exercise in Older Women, Clin. Nutr. source

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    Premisecitation

    Glutamine supplementation prevents glucocorticoid-induced SD rat skeletal muscle atrophy and increases muscle mass, partially through inhibiting myostatin.

    “Moreover, glutamine supplementation prevents glucocorticoid-induced SD rats skeletal muscle atrophy and increases muscle mass, partially through inhibiting the expression of myostatin.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [37] Salehian, 2006, The Effect of Glutamine on Prevention of Glucocorticoid-Induced Skeletal Muscle Atrophy Is Associated with Myostatin Suppression, Metabolism source

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    Premisecitation

    Glutamine stimulates protein-synthetic and inhibits protein-degradative signaling pathways in skeletal muscle of diabetic rats.

    “Glutamine is an important amino acid with many functions in the body, such as stimulating protein-synthetic and inhibiting protein-degradative signaling pathways in skeletal muscle of diabetic rats [34].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [34] Lambertucci, A.C., Lambertucci, R.H., Hirabara, S.M., Curi, R., Moriscot, A.S., Alba-Loureiro, T.C., Guimarцëes-Ferreira, L., Levada-Pires, A.C., Vasconcelos, D.A., and Sellitti, D.F. (2012). Glutamine Supplementation Stimulates Protein-Synthetic and Inhibits Protein-Degradative Signaling Pathways in Skeletal Muscle of Diabetic Rats. PLoS ONE, 7. source

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    Premisecitation

    Vitamin D deficiency may contribute to development of muscle atrophy and possible mechanism is related to increased expression of MAFbx and protein degradation.

    “Vitamin D deficiency may contribute to the development of muscle atrophy and the possible mechanism is related to the increased expression of MAFbx and protein degradation [59].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [59] Garcia, 2019, Vitamin D, Muscle Recovery, Sarcopenia, Cachexia, and Muscle Atrophy, Nutrition source

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    Premisecitation

    Vitamin C deficiency causes muscle atrophy in mice, associated with high expression of MAFbx and MuRF1 and overproduction of ROS.

    “Vitamin C deficiency causes muscle atrophy in mice, which is associated with high expression of muscle atrophy gene of MAFbx and MuRF1 and overproduction of ROS.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [56] Takisawa, 2019, Vitamin C Deficiency Causes Muscle Atrophy and a Deterioration in Physical Performance, Sci. Rep. source

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    Premisecitation

    Daily calcium intake was significantly lower in subjects with sarcopenia than in those without, and there is a strong inverse association between daily calcium intake and sarcopenia in non-obese, older Korean adults.

    “The fourth Korea National Health and Nutrition Examination Survey data showed that daily calcium intake was significantly lower (2.7%) in subjects with sarcopenia than in those without (6.3%) and there is a strong inverse association between daily calcium intake and sarcopenia in non-obese, older Korean adults [50].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [50] Seo, 2013, The Association between Daily Calcium Intake and Sarcopenia in Older, Non-Obese Korean Adults: The Fourth Korea National Health and Nutrition Examination Survey (KNHANES IV) 2009, Endocr. J. source

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    Premisecitation

    Oral vitamin D and E supplement preserves muscle mass and strength and enhances quality of life in sarcopenic older adults.

    “A double-blind randomized controlled trial reported that oral vitamin D and E supplement preserves muscle mass and strength and enhances quality of life in sarcopenic older adults [63].”
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    • cites [63] Bo, 2019, A High Whey Protein, Vitamin D and E Supplement Preserves Muscle Mass, Strength, and Quality of Life in Sarcopenic Older Adults: A Double-Blind Randomized Controlled Trial, Clin. Nutr. source

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    Interpretationcitation

    S-allyl cysteine significantly inhibits proteolytic systems and inflammatory/oxidative molecules and plays a crucial role in prevention of skeletal muscle atrophy.

    “Those results illustrate that SAC significantly inhibits the proteolytic systems and inflammatory/oxidative molecules and therefore play a crucial role in the prevention of skeletal muscle atrophy.”
    Quote in the paperSubstantial claim

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    Premisecitation

    N-myristoylated Cblin inhibits dexamethasone-induced atrophy in C2C12 myotubes and increases gastrocnemius muscle wet weight and cross-sectional area in dexamethasone-treated C57BL/6 mice, associated with downregulated MAFbx and MuRF1.

    “For example, N-myristoylated Cblin, a peptide mimetic of tyrosine, inhibits dexamethasone-induced atrophy in C2C12 myotubes and increases gastrocnemius muscle wet weight and cross-sectional area in dexamethasone-treated C57BL/6 mice. The primary mechanism is associated with the downregulated expression of MAFbx and MuRF1 [46].”
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    • cites [46] Ochi, 2015, N-Myristoylated Ubiquitin Ligase Cbl-b Inhibitor Prevents on Glucocorticoid-Induced Atrophy in Mouse Skeletal Muscle, Arch. Biochem. Biophys. source

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    Premisecitation

    Laminin mimetic peptide nanofibers promote activation of satellite cell in skeletal muscle and accelerate regeneration myofibrillar following acute muscle injury in SD rats.

    “Laminin mimetic peptide nanofibers significantly promote the activation of satellite cell in skeletal muscle and accelerate the regeneration myofibrillar following acute muscle injury in SD rats [47].”
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    • cites [47] Uzunalli, 2017, Laminin Mimetic Peptide Nanofibers Regenerate Acute Muscle Defect, Acta Biomater. source

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    Premisecitation

    Oral taurine attenuates diquat-induced muscle damage and suppresses MAFbx and MuRF1 gene expression in skeletal muscle of piglets.

    “Furthermore, oral supplementation of taurine attenuates diquat-induced muscle damage and suppresses the gene expression of muscle atrophy-related genes (MAFbx and MuRF1) in the skeletal muscle of piglets [40].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [40] Wen, 2020, L-Glutamine Improves Skeletal Muscle Cell Differentiation and Prevents Myotube Atrophy after Cytokine, J. Anim. Sci. Biotechnol. source

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    Premisecitation

    Supplementation with a combination of fish oil and selenium increases soleus and gastrocnemius muscle mass and reduces IL-6, TNF-α, and myostatin levels in gastrocnemius of tumor-bearing C57BL/6 mice.

    “Besides, supplementation with a combination of fish oil and selenium increase soleus and gastrocnemius muscle mass and reduces IL-6, TNF-α, and myostatin levels in gastrocnemius of tumor-bearing C57BL/6 mice [55].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [55] Wang, 2015, Skeletal Muscle Atrophy Is Attenuated in Tumor-Bearing Mice under Chemotherapy by Treatment with Fish Oil and Selenium, Oncotarget source

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    Premisecitation

    S-allyl cysteine alleviates mass loss and increases cross-sectional area of muscle in Swiss albino mice.

    “They also demonstrated that SAC alleviates mass loss and increases cross-sectional area of muscle on Swiss albino mice [43].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [43] Gupta, 2020, S-Allyl Cysteine: A Potential Compound against Skeletal Muscle Atrophy, Biochim. Biophys. Acta Gen. Subj. source

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    Premisecitation

    S-allyl cysteine suppresses rise in cytokines (TNF-α, IL-6, myostatin) and protects myotubes from H2O2-induced protein loss in C2C12 myotubes.

    “Gupta et al. reported that SAC suppresses the rise in cytokines levels (TNF-α, IL-6, and myostatin) and protects myotubes from H2O2-induced protein loss in C2C12 myotubes.”
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    • cites [43] Gupta, 2020, S-Allyl Cysteine: A Potential Compound against Skeletal Muscle Atrophy, Biochim. Biophys. Acta Gen. Subj. source

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    Premisecitation

    Oral gavage of creatine to Wistar rats increases muscle mass and protein level of 4E-BP1 in extensor digitorum longus and prevents hindlimb suspension-induced muscle atrophy.

    “In a separate study, Marzuca-Nassr et al. reported that oral gavage of creatine to Wistar rats increases the muscle mass and the protein level of 4E-BP1 in extensor digitorum longus and prevents hindlimb suspension-induced muscle atrophy [42].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [42] Fortes, 2019, Short-Term Creatine Supplementation Changes Protein Metabolism Signaling in Hindlimb Suspension, Braz. J. Med. Biol. Res. source

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    Interpretationreasoning

    Vitamins have therapeutic potential for inhibiting muscle atrophy and inducing muscle hypertrophy, with main mechanism associated with inhibition of oxidative stress, activation of mitochondrial biogenesis, and suppression of expression of genes related to muscular atrophy.

    “Therefore, these results suggest that vitamins have the therapeutic potential for inhibiting muscle atrophy and inducing muscle hypertrophy. The main mechanism is associated with the inhibition of oxidative stress, the activation of mitochondrial biogenesis, and the suppression the expression of genes related to muscular atrophy.”
    Quote in the paperSubstantial claim

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    Premisecitation

    Curcumin increases number of muscle fibers and decreases muscle fibers proteolysis in SD rats under hypobaric hypoxia, leading to enhanced muscle mass and improved physical performance.

    “Curcumin increases the number of muscle fibers and decreases muscle fibers proteolysis in SD rats under hypobaric hypoxia, leading to enhanced muscle mass and improved physical performance [85].”
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    • cites [85] Chaudhary, 2019, High Altitude Mediated Skeletal Muscle Atrophy: Protective Role of Curcumin, Biochimie source

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    Premisecitation

    Royal jelly attenuates denervation-induced skeletal muscle atrophy in C57BL/6J mice and stimulates myoblast proliferation and differentiation of C2C12 cells.

    “It attenuates denervation-induced skeletal muscle atrophy in C57BL/6J mice and stimulates myoblast proliferation and differentiation of C2C12 cells [81].”
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    • cites [81] Shirakawa, T., Miyawaki, A., Matsubara, T., Okumura, N., Okamoto, H., Nakai, N., Rojasawasthien, T., Morikawa, K., Inoue, A., and Goto, A. (2020). Daily Oral Administration of Protease-Treated Royal Jelly Protects against Denervation-Induced Skeletal Muscle Atrophy. Nutrients, 12. source

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    Premisecitation

    Resveratrol improves muscle atrophy and enhances grip strength and running distance in streptozotocin-induced diabetic mice, associated with suppression of MuRF-1 and cleaved caspase-3.

    “Resveratrol improves muscle atrophy and enhances grip strength and running distance in streptozotocin-induced diabetic mice, which is associated with a suppression of MuRF-1 and cleaved caspase-3.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [86] Wang, 2018, Resveratrol Improves Muscle Atrophy by Modulating Mitochondrial Quality Control in STZ-Induced Diabetic Mice, Mol. Nutr. Food Res. source

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  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Combination of vitamin C and vitamin E can efficaciously eliminate water-soluble and fat-soluble free radicals at the same time, preventing free radicals from causing oxidative damage to the cell membrane.

    “It was thought that the combination of vitamin C and vitamin E can efficaciously eliminate water-soluble and fat-soluble free radicals at the same time, preventing free radicals from causing oxidative damage to the cell membrane [64].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [64] Geng, R., Kang, S.-G., Huang, K., and Tong, T. (2021). Boosting the Photoaged Skin: The Potential Role of Dietary Components. Nutrients, 13. source

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  • May combine two claims.

    Premisecitation

    Long-term administration of nicotinamide mononucleotide enhances age-associated C57BL/6N mice locomotor activity and enhances mitochondrial respiratory capacity in skeletal muscle.

    “Long-term administration of nicotinamide mononucleotide enhances age-associated C57BL/6N mice locomotor activity and enhances mitochondrial respiratory capacity in skeletal muscle [70].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [70] Mills, 2016, Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice, Cell Metab. source

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  • May combine two claims.

    Premisecitation

    CoQ10 administration ameliorates disuse-induced skeletal muscle atrophy via activation of mitochondrial biogenesis and amelioration of oxidative stress in SD rats, and reduces MuRF-1, MAFbx, and FoxO3 expression.

    “Similarly, Liu et al. reported that CoQ10 administration ameliorates disuse-induced skeletal muscle atrophy via the activation of mitochondrial biogenesis and the amelioration of oxidative stress in SD rats. In addition, the expression of MuRF-1, MAFbx, and Forkhead box O3 (FoxO3) were reduced by the CoQ10 [68].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [68] Liu, 2014, Reloading Functionally Ameliorates Disuse-Induced Muscle Atrophy by Reversing Mitochondrial Dysfunction, and Similar Benefits Are Gained by Administering a Combination of Mitochondrial Nutrients, Free Radic. Biol. Med. source

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  • May combine two claims.

    Premisecitation

    Pomegranate extract prevents muscle mass loss induced by TNF-α injection in C57BL/6 mice, associated with inhibition of oxidative stress, NF-κB, and ubiquitin-proteasome system and activation of Akt/mTOR signaling.

    “Pomegranate is rich in a variety of phenolic compounds and its extract prevents muscle mass loss induced by TNF-α injection in C57BL/6 mice. The mechanism is associated with the inhibition of oxidative stress, NF-κB, and the ubiquitin-proteasome system and the activation of Akt/mTOR signaling [93].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [93] Rodriguez, 2017, Pomegranate Extract Prevents Skeletal Muscle of Mice against Wasting Induced by Acute TNF-α Injection, Mol. Nutr. Food Res. source

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  • Classified as probably not a substantial claim.

    Interpretationreasoning

    Interaction between structurally different antioxidant compounds may provide more comprehensive protection against oxidative stress.

    “This could be due to the fact that the interaction between structurally different antioxidant compound may provide more comprehensive protection against oxidative stress.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationnone given

    The primary mechanism of polyphenols' anti-atrophy effect is related to inhibition of oxidative stress, inflammation, and muscle atrophy related genes and activation of IGF-1 signaling pathway.

    “The primary mechanism is related to the inhibition of oxidative stress, inflammation, and muscle atrophy related genes and the activation of IGF-1 signaling pathway.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Oligonol alleviates palmitate-induced senescent phenotype in C2C12 myotubes and suppresses the expression of MAFbx and MuRF1.

    “Oligonol alleviates palmitate-induced senescent phenotype in C2C12 myotubes and suppresses the expression of MAFbx and MuRF1.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [99] Liu, H.W., Chen, Y.J., Chang, Y.C., and Chang, S.J. (2017). Oligonol, a Low-Molecular Weight Polyphenol Derived from Lychee, Alleviates Muscle Loss in Diabetes by Suppressing Atrogin-1 and MuRF1. Nutrients, 9. source

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  • May combine two claims.

    Premisecitation

    Dietary supplementation of epicatechin prevents muscle loss and regulates quantity and quality of muscle by increasing MyoD, superoxide dismutase, and catalase in biceps femoris and decreasing FoxO3a, myostatin, and MuRF1 in soleus of ICR mice.

    “Dietary supplementation of epicatechin prevents muscle loss and regulates the quantity and quality of muscle by increasing the expression of MyoD, superoxide dismutase, and catalase in the biceps femoris muscle and decreasing the expression of FoxO3a, myostatin, and MuRF1 in the soleus muscle of ICR mice [91].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [91] Hong, 2020, Tannase-Converted Green Tea Extract with High (−)-Epicatechin Inhibits Skeletal Muscle Mass in Aged Mice, Evid. Based Complement. Altern. Med. source

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  • May combine two claims.

    Premisecitation

    Resveratrol inhibits mitophagy and increases mitochondrial biogenesis in skeletal muscle of diabetic mice.

    “Besides, it also inhibits mitophagy and increases mitochondrial biogenesis in skeletal muscle of diabetic mice [86].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [86] Wang, 2018, Resveratrol Improves Muscle Atrophy by Modulating Mitochondrial Quality Control in STZ-Induced Diabetic Mice, Mol. Nutr. Food Res. source

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  • May combine two claims.

    Premisecitation

    Intraperitoneal administration of epicatechin gallate to C57BL/6 mice stimulates muscle satellite cell activation and differentiation, which is necessary for muscle regeneration.

    “Intraperitoneally administration of epicatechin gallate to C57BL/6 mice stimulates muscle satellite cell activation and differentiation, which is necessary for muscle regeneration.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [90] Kim, 2017, Catechins Activate Muscle Stem Cells by Myf5 Induction and Stimulate Muscle Regeneration, Biochem. Biophys. Res. Commun. source

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  • May combine two claims.

    Premisecitation

    Corylifol A inhibits dexamethasone-induced muscle atrophy in C2C12 cells, related to inhibition of catabolic pathways and activation of the anabolic pathway.

    “It also inhibits dexamethasone-induced muscle atrophy in C2C12 cells, which is related to the inhibition of catabolic pathways and the activation of the anabolic pathway [101].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [101] Han, Y., Lee, H., Li, H., and Ryu, J.H. (2020). Corylifol A from Psoralea corylifolia L. Enhances Myogenesis and Alleviates Muscle Atrophy. Int. J. Mol. Sci., 21. source

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  • May combine two claims.

    Premisecitation

    In C. elegans, urolithin A extends lifespan and improves muscle health.

    “In C. elegans, urolithin A, as an autophagy inducer, extends lifespan and improves muscle heath [95].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [95] Ryu, 2016, Urolithin a Induces Mitophagy and Prolongs Lifespan in C. elegans and Increases Muscle Function in Rodents, Nat. Med. source

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  • May combine two claims.

    Premisecitation

    In vivo, urolithin B reduces muscle weight loss induced by denervation and inhibits protein degradation by downregulating FoxO1, FoxO3a, MAFbx, and MuRF1.

    “In vivo, urolithin B reduces muscle weight loss induced by denervation and inhibit protein degradation by downregulating the mRNA expression of atrophy-related genes, such as FoxO1, FoxO3a, MAFbx and MuRF1 [96].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [96] Rodriguez, 2017, Urolithin B, a Newly Identified Regulator of Skeletal Muscle Mass, J. Cachexia Sarcopenia Muscle source

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  • May combine two claims.

    Premisecitation

    In in vitro and in vivo models, urolithin A induces mitophagy and improves grip strength and overnight running distance.

    “In both in vitro (C2C12 myoblasts and Mode-K intestinal cells) and in vivo (aging and HFD-fed C57BL/6J mice) models, urolithin A induces mitophagy and improves grip strength and overnight running distance [95].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [95] Ryu, 2016, Urolithin a Induces Mitophagy and Prolongs Lifespan in C. elegans and Increases Muscle Function in Rodents, Nat. Med. source

      Not checked in the free run.

    • Rests on an assumption: Mitochondrial autophagy in aging skeletal muscle plays an important role in promoting muscle health.

  • May combine two claims.

    Premisecitation

    Oral administration of urolithin A improves mitochondrial function and promotes muscle health in the elderly.

    “Moreover, oral administration of urolithin A improves mitochondrial function and promotes muscle health in the elderly [94].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [94] Andreux, 2019, The Mitophagy Activator Urolithin a Is Safe and Induces a Molecular Signature of Improved Mitochondrial and Cellular Health in Humans, Nat. Metab. source

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  • May combine two claims.

    Premisecitation

    Cryptotanshinone protects against muscle atrophy induced by colon adenocarcinoma CT26 in BALB/c mice and improves myotube atrophy of C2C12 cells, associated with reduced expression of MuRF1 and MAFbx.

    “Cryptotanshinone, a major lipophilic compound found in the root of Danshen, protects against muscle atrophy induced by colon adenocarcinoma CT26 in BALB/c mice and improves myotube atrophy of C2C12 cells, which is associated with the reduced the expression of MuRF1 and MAFbx [122].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [122] Chen, 2020, Cryptotanshinone Prevents Muscle Wasting in CT26-Induced Cancer Cachexia through Inhibiting Stat3 Signaling Pathway, J. Ethnopharmacol. source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The metabolism, bioavailability, and biological activity of flavonoids depend upon the configuration, total number of hydroxyl groups, and substitution of functional groups about their nuclear structure.

    “For example, the metabolism, bioavailability, and biological activity of flavonoids depend upon the configuration, total number of hydroxyl groups, and substitution of functional groups about their nuclear structure [109].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [109] Li, 2021, Natural Products in Agarwood and Aquilaria Plants: Chemistry, Biological Activities and Biosynthesis, Nat. Prod. Rep. source

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  • May combine two claims.

    Premisecitation

    Astragalus polysaccharides promote cell proliferation and inhibit cell apoptosis in H2O2-induced cell damage in C2C12 cells.

    “Besides, Astragalus polysaccharides also promote cell proliferation and inhibit cell apoptosis in H2O2-induced cell damage in C2C12 cells [126].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [126] Lu, 2013, Astragalus Polysaccharide Improves Muscle Atrophy from Dexamethasone- and Peroxide-Induced Injury in Vitro, Int. J. Biol. Macromol. source

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  • May combine two claims.

    Premisecitation

    Silibinin increases protein content and decreases MuRF1 and MAFbx expression in skeletal muscle of pancreatic cancer NCr-nu/nu mice.

    “Shukla et al. provided compelling evidence that silibinin increases the protein content and decreases MuRF1 and MAFbx expression in skeletal muscle of pancreatic cancer NCr-nu/nu mice [120].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [120] Shukla, 2015, Silibinin-Mediated Metabolic Reprogramming Attenuates Pancreatic Cancer-Induced Cachexia and Tumor Growth, Oncotarget source

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  • May combine two claims.

    Premisecitation

    Dietary supplement of fucoidan can prevent cancer cachexia-associated muscle atrophy in BALB/c mice during chemotherapy, associated with suppressed FoxO3a, MuRF1, and MAFbx and enhanced IGF-1-dependent protein synthesis.

    “Chen et al. reported that dietary supplement of fucoidan can prevent cancer cachexia-associated muscle atrophy in BALB/c mice during chemotherapy, which may be associated with suppressed muscle wasting-related genes including FoxO3a, MuRF1, and MAFbx and enhanced IGF-1-dependent protein synthesis [128].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [128] Chen, 2016, Combined Administration of Fucoidan Ameliorates Tumor and Chemotherapy-Induced Skeletal Muscle Atrophy in Bladder Cancer-Bearing Mice, Oncotarget source

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  • May combine two claims.

    Premisecitation

    Magnoflorine increases expression of MyoD and MHC and stimulates myoblast differentiation via the activation of p38 MAPK and Akt signaling in C2C12 myotubes.

    “Magnoflorine increases expression of MyoD and MHC and subsequently stimulates myoblast differentiation via the activation of p38 MAPK and Akt signaling in C2C12 myotubes [132].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [132] Lee, 2017, Isoquinoline Alkaloids from Coptis Japonica Stimulate the Myoblast Differentiation Via P38 MAP-Kinase and Akt Signaling Pathway, Bioorg. Med. Chem. Lett. source

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  • May combine two claims.

    Premisecitation

    Dietary supplementation of apigenin ameliorates obesity-induced skeletal muscle atrophy and increases exercise capacity.

    “Choi et al. reported that dietary supplementation of apigenin ameliorates the obesity-induced skeletal muscle atrophy and increases the exercise capacity.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [110] Choi, 2017, Apigenin Ameliorates the Obesity-Induced Skeletal Muscle Atrophy by Attenuating Mitochondrial Dysfunction in the Muscle of Obese Mice, Mol. Nutr. Food Res. source

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  • May combine two claims.

    Premisecitation

    The underlying mechanisms of Aureobasidium pullulans polysaccharides involve increased expression of genes related to muscle protein synthesis (Akt and PI3K) and inhibition of genes involved in muscle protein degradation (MAFbx, MuRF1, myostatin, and sirtuin-1).

    “The underlying mechanisms involve the increased expression of genes related to muscle protein synthesis (Akt and PI3K) and the inhibition of genes involved in muscle protein degradation (MAFbx, MuRF1, myostatin, and sirtuin-1) [127].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [127] Lim, 2018, Extracellular Polysaccharides Purified from Aureobasidium Pullulans SM-2001 (Polycan) Inhibit Dexamethasone-Induced Muscle Atrophy in Mice, Int. J. Mol. Med.

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Oral administration of fucoidan for 4 weeks improves cross-sectional area of extensor digitorum longus fibers and soleus fibers and enhances the expression of MHC in gastrocnemius muscles in C57BL/6 mice.

    “Oral administration of fucoidan for 4 weeks improves cross-sectional area of extensor digitorum longus fibers and soleus fibers and enhances the expression of MHC in gastrocnemius muscles muscle in C57BL/6 mice [130].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [130] McBean, 2021, Oral Fucoidan Improves Muscle Size and Strength in Mice, Physiol. Rep. source

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  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Flavonoids are characterized by a flavone ring and exert anti-inflammation and antioxidant properties.

    “Flavonoids, a class of benzo-gamma-pyrone derivatives abundant in foods and plants, are characterized by a flavone ring and exert anti-inflammation and antioxidant properties [108].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [108] Kawser Hossain, M., Abdal Dayem, A., Han, J., Yin, Y., Kim, K., Kumar Saha, S., Yang, G.M., Choi, H.Y., and Cho, S.G. (2016). Molecular Mechanisms of the Anti-Obesity and Anti-Diabetic Properties of Flavonoids. Int. J. Mol. Sci., 17. source

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  • May combine two claims.

    Premisecitation

    In an in vitro model of C2C12 cells, Dioscorea nipponica extracts inhibits TNF-α-induced atrophy and promotes myoblast differentiation.

    “In vitro model of C2C12 cells, Dioscorea nipponica extracts inhibits TNF-α-induced atrophy and promotes myoblast differentiation [129].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [129] Park, 2020, Dioscorea Nipponica Extracts Enhance Recovery from Skeletal Muscle Atrophy by Suppressing NF-κB Expression, J. Funct. Foods source

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  • May combine two claims.

    Premisecitation

    Dietary supplementation of α-ionone improves the loss of skeletal muscle induced by HFD in C57BL/6N mice and prevents C2C12 myotubes from palmitic acid-induced atrophy via cyclic adenosine monophosphate signaling.

    “Dietary supplementation of α-ionone, a naturally occurring flavoring agent in violets and blackberries, improves the loss of skeletal muscle induced by HFD in C57BL/6N mice and prevents C2C12 myotubes from palmitic acid-induced atrophy via cyclic adenosine monophosphate signaling [121].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [121] Tong, 2019, α-Ionone Attenuates High-Fat Diet-Induced Skeletal Muscle Wasting in Mice Via Activation of cAMP Signaling, Food Funct. source

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  • May combine two claims.

    Premisecitation

    Ursolic acid reduces fasting- and denervation-induced muscle atrophy by inhibiting the mRNA expression of MAFbx and MuRF1 and induces skeletal muscle hypertrophy in SD rats.

    “Ursolic acid, a pentacyclic triterpenoid abundant in apples, reduces fasting- and denervation-induced muscle atrophy by inhibiting the mRNA expression of MAFbx and MuRF1 and induces skeletal muscle hypertrophy in SD rats [145].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [145] Kunkel, 2011, mRNA Expression Signatures of Human Skeletal Muscle Atrophy Identify a Natural Compound That Increases Muscle Mass, Cell Metab. source

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  • May combine two claims.

    Premisecitation

    Apple pomace extract increases the expression of IGF-1, Akt, mTOR, and S6K1 and reduces the expression of MAFbx and MuRF1 in C2C12 myotubes.

    “Similarly, it increases the expression of IGF-1, Akt, mTOR, and S6K1 and reduces the expression of MAFbx and MuRF1 in C2C12 myotubes [147].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [147] Jeong, 2015, Apple Pomace Extract Improves Endurance in Exercise Performance by Increasing Strength and Weight of Skeletal Muscle, J. Med. Food source

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  • May combine two claims.

    Premisecitation

    Mountain ginseng attenuates the expression of MuRF1, MAFbx, and FoxO3a and promotes differentiation of myoblasts in dexamethasone-induced L6 cells.

    “Mountain ginseng, mainly including ginsenoside Rb1 followed by ginsenoside Rb2, attenuates the expression of MuRF1, MAFbx, and FoxO3a and promotes differentiation of myoblasts in dexamethasone-induced L6 cells.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [151] Seok, 2021, Mountain Ginseng Inhibits Skeletal Muscle Atrophy by Decreasing Muscle Ring finger Protein-1 and Atrogin1 through Forkhead Box O3 in L6 Myotubes, J. Ethnopharmacol. source

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  • May combine two claims.

    Premisecitation

    Ginsenoside Rg3 enhances mitochondrial functions and upregulates the expression of PGC1α, Nrf1, and Tfam, and thereby protects TNF-α-induced myotube atrophy in C2C12 cells.

    “Furthermore, ginsenoside Rg3 enhances mitochondrial functions and upregulates the expression of PGC1α, Nrf1, and Tfam, and thereby protects TNF-α-induced myotube atrophy in C2C12 cells [149].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [149] Lee, 2019, Ginsenoside Rg3 Upregulates Myotube Formation and Mitochondrial Function, Thereby Protecting Myotube Atrophy Induced by Tumor Necrosis Factor-Alpha, J. Ethnopharmacol. source

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  • May combine two claims.

    Premisecitation

    Ginsenoside Rg3 enhances myotube growth and suppresses the expression of MuRF1 and MAFbx in TNF-α-induced muscle atrophy of C2C12 myotubes via the activation of Akt/mTOR signaling pathway.

    “Like ginsenoside Rg1, ginsenoside Rg3 enhances myotube growth and suppresses the expression of MuRF1, MAFbx in TNF-α-induced muscle atrophy of C2C12 myotubes via the activation of Akt/mTOR signaling pathway.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [149] Lee, 2019, Ginsenoside Rg3 Upregulates Myotube Formation and Mitochondrial Function, Thereby Protecting Myotube Atrophy Induced by Tumor Necrosis Factor-Alpha, J. Ethnopharmacol. source

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  • May combine two claims.

    Premisecitation

    Tetrahydropalmatine enhances myoblast differentiation through the activation of p38MAPK and MyoD and has potential as a therapeutic candidate to prevent fibrosis and improve muscle regeneration and repair in C2C12 myotubes.

    “Tetrahydropalmatine, another compound isolated from Corydalis turtschaninovii, enhances myoblast differentiation through the activation of p38MAPK and MyoD and has the potential as a therapeutic candidate to prevent fibrosis and improve muscle regeneration and repair in C2C12 myotubes [135].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [135] Lee, 2014, Tetrahydropalmatine Promotes Myoblast Differentiation through Activation of p38MAPK and MyoD, Biochem. Biophys. Res. Commun. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Dietary supplement with apple pomace extracts significantly increases skeletal muscle strength and weight, related to upregulation of IGF-1 genes and downregulation of MAFbx and MuRF1 in hindlimb skeletal muscle of C57BL/6N mice.

    “Dietary supplement with apple pomace extracts significantly increases skeletal muscle strength and weight, which is related to the upregulation the expression of IGF-1 genes and downregulation of the expression of MAFbx and MuRF1 in hindlimb skeletal muscle of C57BL/6N mice.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [147] Jeong, 2015, Apple Pomace Extract Improves Endurance in Exercise Performance by Increasing Strength and Weight of Skeletal Muscle, J. Med. Food source

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  • May combine two claims.

    Premisecitation

    Canadine stimulates myoblast differentiation through the activation of p38 MAPK and Akt signaling and protects against C2C12 myotube atrophy induced by conditioned media from CT26 colon carcinoma culture by downregulating MAFbx and MuRF1.

    “Canadine, an important alkaloid of Corydalis turtschaninovii, stimulates myoblast differentiation through the activation of p38 MAPK and Akt signaling and protects against C2C12 myotube atrophy induced by conditioned media from CT26 colon carcinoma culture by downregulating the muscle specific-E3 ligases, MAFbx and MuRF1 [134].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [134] Lee, H., Lee, S.J., Bae, G.U., Baek, N.I., and Ryu, J.H. (2017). Canadine from Corydalis turtschaninovii Stimulates Myoblast Differentiation and Protects against Myotube Atrophy. Int. J. Mol. Sci., 18. source

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  • May combine two claims.

    Premisecitation

    Tomatidine improves muscle function during aging in C. elegans by activating the Nrf2/Protein skinhead-1 pathway and upregulating mitophagy and antioxidant cellular defenses.

    “Besides, it improves muscle function during aging in C. elegans by activating the Nrf2/Protein skinhead-1 pathway and upregulating mitophagy and antioxidant cellular defenses [137].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [137] Fang, 2017, Tomatidine Enhances Lifespan and Healthspan in C. elegans through Mitophagy Induction Via the SKN-1/Nrf2 Pathway, Sci. Rep. source

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  • May combine two claims.

    Premisecitation

    Tinospora cordifolia extract rich in alkaloids compounds supplementation improves muscle atrophy induced by sciatic denervation of Swiss albino mice and increases myogenic differentiation of C2C12 myoblasts by alleviating oxidative stress and inflammation.

    “Tinospora cordifolia extract rich in alkaloids compounds supplementation improves muscle atrophy induced by sciatic denervation of Swiss albino mice and increases myogenic differentiation of C2C12 myoblasts by alleviating oxidative stress and inflammation [143].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [143] Sharma, 2020, Tinospora Cordifolia Protects from Skeletal Muscle Atrophy by Alleviating Oxidative Stress and Inflammation Induced by Sciatic Denervation, J. Ethnopharmacol. source

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  • May combine two claims.

    Premisecitation

    Tomatidine stimulates skeletal muscle hypertrophy and increases strength and exercise capacity.

    “Moreover, tomatidine stimulates skeletal muscle hypertrophy and increases strength and exercise capacity [136].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [136] Dyle, 2014, Systems-Based Discovery of Tomatidine as a Natural Small Molecule Inhibitor of Skeletal Muscle Atrophy, J. Biol. Chem. source

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  • May combine two claims.

    Premisecitation

    In SD rats exposed to dexamethasone, mountain ginseng treatment attenuates skeletal muscle atrophy and inhibits the expression of MuRF1 and MAFbx.

    “In SD rats exposed with dexamethasone, mountain ginseng treatment attenuates skeletal muscle atrophy and inhibits the expression of MuRF1 and MAFbx [151].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [151] Seok, 2021, Mountain Ginseng Inhibits Skeletal Muscle Atrophy by Decreasing Muscle Ring finger Protein-1 and Atrogin1 through Forkhead Box O3 in L6 Myotubes, J. Ethnopharmacol. source

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  • May combine two claims.

    Premisecitation

    In C2C12 myoblasts and 3T3-L1 cells, Arctium lappa L. fruit extract decreases the expression of muscle degradation factors (MAFbx and MuRF1) and increases adipocytes differentiation factors, respectively.

    “In C2C12 myoblasts and 3T3-L1 cells, it decreases the expression of muscle degradation factors (MAFbx and MuRF1) and increases adipocytes differentiation factors, respectively [157].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [157] Han, Y.H., Mun, J.G., Jeon, H.D., Yoon, D.H., Choi, B.M., Kee, J.Y., and Hong, S.H. (2020). The Extract of Arctium lappa L. Fruit (Arctii Fructus) Improves Cancer-Induced Cachexia by Inhibiting Weight Loss of Skeletal Muscle and Adipose Tissue. Nutrients, 12. source

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  • May combine two claims.

    Premisecitation

    Tomatidine stimulates mTORC1 signaling resulting in the accumulation of protein and mitochondria, and ultimately cell growth in C2C12 myoblasts and human skeletal myotubes.

    “Tomatidine also stimulates mTORC1 signaling resulting in the accumulation of protein and mitochondria, and ultimately, cell growth in C2C12 myoblasts and human skeletal myotubes.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [136] Dyle, 2014, Systems-Based Discovery of Tomatidine as a Natural Small Molecule Inhibitor of Skeletal Muscle Atrophy, J. Biol. Chem. source

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  • May combine two claims.

    Premisecitation

    TGF-β regulates several processes in skeletal muscle disease including inhibition of myogenesis, diminution of regeneration, and induction of muscle atrophy.

    “TGF-β, a classical modulator of skeletal muscle, regulates several processes in skeletal muscle disease including inhibition of myogenesis, diminution of regeneration, and induction of muscle atrophy.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [140] Abrigo, 2015, Apocynin Inhibits the Upregulation of TGF-β1 Expression and ROS Production Induced by TGF-β in Skeletal Muscle Cells, Phytomedicine source

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  • May combine two claims.

    Premisecitation

    Fucoxanthin increases tibialis anterior muscle and gastrocnemius muscle weight and protects against dexamethasone-induced muscle atrophy through reducing oxidative stress in tibialis anterior muscle in ICR mice.

    “Fucoxanthin, a carotenoid produced by Undaria pinnatifida and Phaeodactylum tricornutum, increases tibialis anterior muscle and gastrocnemius muscle weight and protects against dexamethasone-induced muscle atrophy through reducing oxidative stress in tibialis anterior muscle in ICR mice [156].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [156] Yoshikawa, M., Hosokawa, M., Miyashita, K., Nishino, H., and Hashimoto, T. (2021). Effects of Fucoxanthin on the Inhibition of Dexamethasone-Induced Skeletal Muscle Loss in Mice. Nutrients, 13. source

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  • May combine two claims.

    Premisecitation

    Ginsenoside Rg1 increases the viability of mouse C2C12 myoblast cells and inhibits the expression of MAFbx and MuRF1 in the starvation-induced muscle atrophy model.

    “For example, ginsenoside Rg1, a primary active ingredient in Panax ginseng, increases the viability of mouse C2C12 myoblast cells and inhibits the expression of MAFbx and MuRF1 in the starvation-induced muscle atrophy model.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [148] Li, 2017, Ginsenoside Rg1 Prevents Starvation-Induced Muscle Protein Degradation Via Regulation of AKT/mTOR/FoxO Signaling in C2C12 Myotubes, Exp. Ther. Med. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Ursolic acid and low-intensity treadmill exercise significantly improves mass of tibialis anterior and gastrocnemius muscles and decreases atrophy-related gene expression of MuRF1 and MAFbx in SD rats induced by hind limb immobilization.

    “Meanwhile, ursolic acid and low-intensity treadmill exercise significantly improves mass of tibialis anterior and gastrocnemius muscles and decreases atrophy-related gene expression of MuRF1 and MAFbx in SD rats induced by hind limb immobilization [146].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [146] Kim, 2018, Concurrent Treatment with Ursolic Acid and Low-Intensity Treadmill Exercise Improves Muscle Atrophy and Related Outcomes in Rats, Korean J. Physiol. Pharmacol. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationnone given

    Knowledge regarding the mechanisms of probiotics is unclear and lacking, while probiotics exert beneficial effects on skeletal muscle atrophy.

    “Compared with the above-mentioned dietary nutrients and phytochemicals including polyphenols, flavonoids, polysaccharides, alkaloids, and triterpenoids, knowledge regarding the mechanisms of probiotics is unclear and lacking, while probiotics exert beneficial effect on skeletal muscle atrophy.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Prebiotics is known to alter the composition and/or activity of the intestinal microbiota and bring possible benefits to the individual's muscle health.

    “In addition, prebiotics is known to alter the composition and/or activity of the intestinal microbiota and bring possible benefits to the individual’s muscle health.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [165] Buigues, C., Fernández-Garrido, J., Pruimboom, L., Hoogland, A.J., Navarro-Martínez, R., Martínez-Martínez, M., Verdejo, Y., Mascarós, M.C., Peris, C., and Cauli, O. (2016). Effect of a Prebiotic Formulation on Frailty Syndrome: A Randomized, Double-Blind Clinical Trial. Int. J. Mol. Sci., 17. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In ICR mice, oral administration of Lactobacillus plantarum TWK10 for six weeks increases muscle mass and improves exercise performance.

    “In ICR mice, oral administration of Lactobacillus plantarum TWK10 for six weeks increases muscle mass and improves exercise performance [159].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [159] Chen, Y.M., Wei, L., Chiu, Y.S., Hsu, Y.J., Tsai, T.Y., Wang, M.F., and Huang, C.C. (2016). Lactobacillus plantarum TWK10 Supplementation Improves Exercise Performance and Increases Muscle Mass in Mice. Nutrients, 8. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationcitation

    Lactobacillus could protect muscle against atrophy and its mechanism is related to decreased systemic inflammation and increased muscle mass.

    “Those results suggest that Lactobacillus could protect muscle against atrophy and its mechanism is related to decreased systemic inflammation and increased muscle mass.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationnone given

    The primary mechanism of phytochemicals includes enhancement of myoblast differentiation, prevention of muscle protein degradation, promotion of protein synthesis and myogenesis, anti-inflammation, anti-oxidation, and downregulation of atrophy-related gene expression.

    “Their primary mechanism includes the enhancement of myoblast differentiation, prevention of muscle protein degradation, the promotion of protein synthesis and myogenesis, anti-inflammation, anti-oxidation, and the downregulation of atrophy-related gene expression.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    When transplanting the gut microbiota from pathogen-free mice into germ-free mice, the skeletal muscle atrophy markers are significantly reduced, and the skeletal muscle mass and oxidative metabolic capacity are improved in C57BL/6J male mice.

    “However, when transplanting the gut microbiota from pathogen-free mice into germ-free mice, the skeletal muscle atrophy markers are significantly reduced, and the skeletal muscle mass and oxidative metabolic capacity are improved in C57BL/6J male mice [166], suggesting that gut microbiota may serve an essential role in preventing muscle atrophy.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [166] Lahiri, 2019, The Gut Microbiota Influences Skeletal Muscle Mass and Function in Mice, Sci. Transl. Med. source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationnone given

    There is little evidence supporting the structure-function relationship of phytochemicals in skeletal muscle atrophy.

    “In addition, there is little evidence supporting the structure-function relationship of phytochemicals in skeletal muscle atrophy.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Yogurt or fermented milk contains different combinations of probiotics including Lactobacillus bulgaricus, Lactobacillus delbrueckii, and Bifidobacterium bifidum.

    “For example, the yogurt or fermented milk contains different combinations of probiotics including Lactobacillus bulgaricus, Lactobacillus delbrueckii, and Bifidobacterium bifidum [162].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [162] Kok, 2018, Yogurt and other fermented foods as sources of health-promoting bacteria, Nutr. Rev. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    The efficacy and molecular mechanisms of most phytochemicals have been examined only in preclinical trials, either in vitro or in vivo, so clinical evidence is not sufficient and is urgently needed.

    “Nevertheless, because the efficacy and molecular mechanisms of most phytochemicals have been examined only in preclinical trials, either in vitro or in vivo, the clinical evidence is not sufficient and is therefore urgently needed.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S2 (checkable).

    Interpretationreasoning

    Nutraceuticals with a relevant role in the prevention of muscle protein loss and maintenance of skeletal muscle mass open an important implication in designing appropriate nutritional therapeutic approaches for skeletal muscle atrophy and other muscle health problems.

    “Nutraceuticals with a relevant role in the prevention of muscle protein loss and maintenance of skeletal muscle mass open an important implication in designing appropriate nutritional therapeutic approaches for skeletal muscle atrophy and other muscle health problem.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: Findings from preclinical models (C2C12 myotubes, mice, rats) about nutraceutical effects on muscle atrophy are relevant to human muscle atrophy.
89 of 89

  • The paper relies on this without support.

    Nutraceuticals are potentially more suitable for long-term use than traditional therapeutic agents.

    “Nutraceuticals with preventive and therapeutic effects against muscle atrophy have recently received increasing attention since they are potentially more suitable for long-term use.”
    “For example, polyphenols, flavonoids, alkaloids, and probiotics show beneficial regulatory effects on muscle cells or tissues and they seem to be potentially more suitable for long-term use than traditional therapeutic agents.”

  • The paper relies on this without support.

    Skeletal muscle atrophy is a relatively understudied and underdeveloped area of biomedical research and still lacks effective pharmacological therapy.

    “On the other hand, despite its broad clinical impact, skeletal muscle atrophy is a relatively understudied and underdeveloped area of biomedical research and still lacks effective pharmacological therapy, which pointing to a large need for effective and new anti-atrophy approaches.”

  • The paper relies on this without support.

    The mechanisms inducing muscle atrophy between the numerous models presented are not identical.

    “The mechanisms inducing muscle atrophy between the numerous models presented are not identical.”

  • The paper relies on this without support.

    Mitochondrial autophagy in aging skeletal muscle plays an important role in promoting muscle health.

    “Mitochondrial autophagy in aging skeletal muscle plays an important role in promoting muscle health.”

  • The paper relies on this without support.

    Findings from preclinical models (C2C12 myotubes, mice, rats) about nutraceutical effects on muscle atrophy are relevant to human muscle atrophy.

    “Although, over the past few decades, the cellular and molecular mechanisms of muscle atrophy have been studied extensively and the beneficial effects of certain nutraceuticals on muscle atrophy in vitro or in vivo have been demonstrated unequivocally, we remain far from having a marketed nutraceutical compounds for muscle atrophy treatment.”

  • The paper relies on this without support.

    Obesity contributes to skeletal muscle atrophy or sarcopenia.

    “Obesity is well known to contribute to skeletal muscle atrophy or sarcopenia.”

  • The paper relies on this without support.

    Most polyphenols act as antioxidants.

    “As most of the polyphenols act as antioxidants, it is therefore necessary to investigate the efficacy of a combination of different polyphenol compounds in preventing skeletal muscle atrophy in the future.”

  • The paper relies on this without support.

    MuRF1 and MAFbx expression levels are valid markers of muscle atrophy or muscle protein degradation.

    “The primary mechanism is related to the inhibition of oxidative stress, inflammation, and muscle atrophy related genes and the activation of IGF-1 signaling pathway.”
8 of 8

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?

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.

  • Taurine claim cites a glutamine study

    Minor

    The piglet claim attributes protection against diquat-induced damage to taurine and cites reference 40. The listed title of reference 40 instead describes L-glutamine treatment after cytokine stress.

  • Table 2 is assigned to both minerals and phytochemicals

    Minor

    The minerals section identifies Table 2 as covering minerals, while the phytochemicals section says the same table presents phytochemical studies.

  • Flavan 3-ol is said to worsen atrophy, but its cited study says it delays atrophy

    Minor

    The text says the cocoa-derived fraction enhances hindlimb-suspension-induced atrophy. The title of the cited study says it delays the progression of that atrophy, reversing the stated effect.

  • Species for the denervation study differ between text and table

    Minor

    The text places the ursolic-acid denervation study in SD rats, but the Table 9 row for the same reference lists C57BL/6 mice.

4 of 4

Cites

Flagged first, then by citations

3 of the 171 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Related

Authors
Wang, Y., Liu, Q., Quan, H., Kang, S.-G., Huang, K., & Tong, T.
Affiliations
  • Beijing Advanced Innovation Center for Food Nutrition and Human Health (CN)
  • Jilin Green Food Engineering Research Institute, Changchun 130022, China
  • Zhejiang Normal University (CN)
  • Mokpo National University (KR)
  • Ministry of Agriculture and Rural Affairs (CN)
Corresponding author
  • Huang, Kunlun
  • Tong, Tao
ORCID
Venue
Nutrients
Publisher
MDPI AG
Published
2021-06-02
Volume
13
Issue
6
Pages
1914
ISSN
2072-6643 (ISSN-L)
DOI
10.3390/nu13061914
PMC
PMC8227811
OpenAlex
W3170817666
Cited by
61
References
171
Citations by year
2026: 7 · 2025: 12 · 2024: 19 · 2023: 12 · 2022: 8 · 2021: 3
FWCI
1.10
Type
journal article
Language
en
Open access
Licence
Locations
  • Nutrients (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Kunlun Huang (The National Key R&D Program of China (grant number: 2017YFC1600901))
  • Yunbo Luo (The 2115 Talent Development Program of China Agricultural University)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
Keywords
nutraceuticals, muscle atrophy, skeletal muscle atrophy, proteostasis, protein degradation, muscle weakness, inflammation, malnutrition, aging, cancer cachexia, sedentary lifestyle, high-fat diet, muscle function recovery, precision medicine
MeSH terms
Amino Acids, Animals, Fatty Acids, Humans, Inflammation, Minerals, Muscular Atrophy, Peptides, Proteins, Vitamins, Databases, Factual, Muscle, Skeletal, Dietary Supplements, Probiotics, Proteolysis, Phytochemicals

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-10.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-10.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

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