Mitochondrial dysfunction and sarcopenia of aging: from signaling pathways to clinical trials
Open accessAbstract
Sarcopenia, the age-related loss of muscle mass and function, imposes a dramatic burden on individuals and society. The development of preventive and therapeutic strategies against sarcopenia is therefore perceived as an urgent need by health professionals and has instigated intensive research on the pathophysiology of this syndrome. The pathogenesis of sarcopenia is multifaceted and encompasses lifestyle habits, systemic factors (e.g., chronic inflammation and hormonal alterations), local environment perturbations (e.g., vascular dysfunction), and intramuscular specific processes. In this scenario, derangements in skeletal myocyte mitochondrial function are recognized as major factors contributing to the age-dependent muscle degeneration. In this review, we summarize prominent findings and controversial issues on the contribution of specific mitochondrial processes - including oxidative stress, quality control mechanisms and apoptotic signaling - on the development of sarcopenia. Extramuscular alterations accompanying the aging process with a potential impact on myocyte mitochondrial function are also discussed. We conclude with presenting methodological and safety considerations for the design of clinical trials targeting mitochondrial dysfunction to treat sarcopenia. Special emphasis is placed on the importance of monitoring the effects of an intervention on muscle mitochondrial function and identifying the optimal target population for the trial. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.
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The primary defect in age-related muscle wasting resides within the structural architecture of the muscle fiber, not chronic systemic inflammation or insulin resistance.
“contemporary human biopsy data confirm that the primary defect resides deep within the structural architecture of the muscle fiber [102,103].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [102]
The Introduction (page unavailable) describes mitochondrial decay within muscle fibers as one of the major factors driving muscle aging. It does not establish that a structural defect is the primary cause or that human biopsy data confirm this. Section 4.1 (page unavailable) also identifies chronic inflammation as a possible contributor to sarcopenia, rather than ruling it out. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThe senescent skeletal muscle nucleolus becomes severely desensitized to mechanical tension, creating a rigid bottleneck that resists widening and accelerating loss of myofibrillar mass.
“The senescent skeletal muscle nucleolus becomes severely desensitized to mechanical tension, creating an extraordinarily rigid bottleneck that resists widening, thereby accelerating the loss of myofibrillar mass [102].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [102]
The Introduction (page unavailable) links myonuclear-domain remodeling to load conditions and aging, but does not discuss the nucleolus or its sensitivity to mechanical tension. A search for nucleolar desensitization, mechanical tension, and rigidity found no passage supporting the claimed bottleneck or its proposed effect on myofibrillar mass. (LLM, conf=0.76)
Experimental — accuracy not yet measuredIntermuscular adipose tissue and intramuscular lipid metabolites can lead to marked impairment in mitochondrial fatty acid oxidation, increased lipolysis, and increased oxidative stress.
“Both intermuscular adipose tissue and intramuscular lipid metabolites can lead to marked impairment in mitochondrial fatty acid oxidation, increased lipolysis, and increased oxidative stress (141, 144, 145).”
From Health Consequences of Sarcopenic Obesity: A Narrative Review (2020) · cites this paper as [145]
Obesity is a risk factor for cardiovascular diseases, metabolic syndrome, type 2 diabetes mellitus, nonalcoholic fatty liver disease, cirrhosis, cancer, osteoarthritis, pulmonary dysfunction, reduced cognitive skills, urinary incontinence, and COVID-19.
“Obesity is a risk factor in developing other diseases such as cardiovascular diseases (atherosclerosis, myocardial infarct, heart failure, and coronary disease), metabolic syndrome, T2DM, NAFLD, cirrhosis, cancer, osteoarthritis, pulmonary dysfunction (e.g., obstructive sleep apnea syndrome), reduced cognitive skills, urinary incontinence, and, more recently, coronavirus disease 2019 (COVID-19) [”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [45]
TNF-α is a proinflammatory cytokine that increases in aging and obesity, promotes protein degradation, decreases protein synthesis, and inhibits myogenic differentiation.
“TNF-α is a proinflammatory cytokine that increases in aging and obesity, promotes protein degradation, decreases protein synthesis, and inhibits myogenic differentiation [14, 45].”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [45]
A decrease in mitochondrial quantity and quality impairs the capacity to generate ATP, activates apoptotic pathways, and induces the loss of muscle fibers.
“Consequently, there is a decrease in mitochondrial quantity and quality, impairing the capacity to generate adenosine triphosphate (ATP), activating apoptotic pathways, and inducing the loss of muscle fibers [45, 75, 84, 86].”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [45]
Mitochondrial dysfunction and oxidative stress play a pivotal role in the pathogenesis of muscle atrophy during aging.
“In the past several years, a growing body of literature has highlighted the pivotal role of mitochondrial dysfunction and oxidative stress in the pathogenesis of muscle atrophy during aging [9–12].”
From Resveratrol prevents sarcopenic obesity by reversing mitochondrial dysfunction and oxidative stress via the PKA/LKB1/AMPK pathway (2019) · cites this paper as [9]
Studies in rodents implicate mitochondrial malfunction and abnormal PCD signaling in sarcopenia.
“The precise mechanisms for sarcopenia are not yet known, however studies in rodents implicate mitochondrial malfunction and abnormal PCD signaling (Marzetti et al., 2013).”
From Programmed cell death in aging (2015) · cites this paper as Marzetti et al., 2013
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Sarcopenia: Aging-Related Loss of Muscle Mass and Function
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on behalf of the SPRINTT Consortium, Marzetti, E., Calvani, R., Tosato, M., Cesari, M., Di Bari, M., Cherubini, A., Collamati, A., D’Angelo, E., Pahor, M., et al. (2017) · Aging Clinical and Experimental Research · doi:10.1007/s40520-016-0704-5 · Cited by 438 · see citing works
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“While early studies in human cohorts attributed age-related muscle wasting to chronic systemic inflammation or insulin resistance, contemporary human biopsy data confirm that the primary defect resides deep within the structural architecture of the muscle fiber [102,103].”
- Authors
- Marzetti, E., Calvani, R., Cesari, M., Buford, T. W., Lorenzi, M., Behnke, B. J., & Leeuwenburgh, C.
- Affiliations
- Università Cattolica del Sacro Cuore (IT)
- National Research Council (IT)
- Inserm (FR)
- University of Florida (US)
- Corresponding author
- Marzetti, Emanuele
- ORCID
- Venue
- The International Journal of Biochemistry & Cell Biology
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 45
- Issue
- 10
- Pages
- 2288-2301
- ISSN
- 1357-2725 (ISSN-L)
- PMC
- PMC3759621
- OpenAlex
- W2046119060
- Cited by
- 627
- References
- 221
- Citations by year
- 2026: 49 · 2025: 65 · 2024: 73 · 2023: 55 · 2022: 67 · 2021: 53 · 2020: 63 · 2019: 34 · 2018: 31 · 2017: 42 · 2016: 29 · 2015: 41 · 2014: 22 · 2013: 2
- FWCI
- 3.39
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The International Journal of Biochemistry & Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Centro Studi Achille e Linda Lorenzon
- Italian Ministry of Economy and Finance to the CNR
- Chair of Excellence of the French Agence Nationale de le Recherche
- NIA (RO1-AG21042, 1P30AG028740)
- NIDDK (RO1-DK090115-01A1)
- University of Florida's Institute on Aging and Claude D. Pepper Older Americans Independence Center
- Topics
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- sarcopenia, mitochondrial dysfunction, skeletal muscle aging, oxidative stress, mitochondrial quality control, apoptosis, chronic inflammation, vascular dysfunction, muscle atrophy, clinical trial design
- MeSH terms
- Aged, Aging, Animals, Humans, Mitochondria, Signal Transduction, Randomized Controlled Trials as Topic, Apoptosis, Oxidative Stress, Sarcopenia, Mitophagy
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