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Models of accelerated sarcopenia: Critical pieces for solving the puzzle of age-related muscle atrophy
Open accessAbstract
Sarcopenia, the age-related loss of skeletal muscle mass, is a significant public health concern that continues to grow in relevance as the population ages. Certain conditions have the strong potential to coincide with sarcopenia to accelerate the progression of muscle atrophy in older adults. Among these conditions are co-morbid diseases common to older individuals such as cancer, kidney disease, diabetes, and peripheral artery disease. Furthermore, behaviors such as poor nutrition and physical inactivity are well-known to contribute to sarcopenia development. However, we argue that these behaviors are not inherent to the development of sarcopenia but rather accelerate its progression. In the present review, we discuss how these factors affect systemic and cellular mechanisms that contribute to skeletal muscle atrophy. In addition, we describe gaps in the literature concerning the role of these factors in accelerating sarcopenia progression. Elucidating biochemical pathways related to accelerated muscle atrophy may allow for improved discovery of therapeutic treatments related to sarcopenia.
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“HIV is also associated with increased circulating concentrations of pro-inflammatory cytokines that can alter protein balance similarly to cancer.109”
From Age-related and disease-related muscle loss: The effect of diabetes, obesity, and other diseases (2014) · cites this paper as [109]
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“Chronic or intermittent hypoxaemia could also affect mitochondrial function in a similar way to age-related muscle loss, leading to oxidative stress, reduced energy availability, and decreased protein synthesis.”
From Age-related and disease-related muscle loss: The effect of diabetes, obesity, and other diseases (2014) · cites this paper as [109]
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“Repeated episodes of ischaemia-reperfusion might be a common pathway associated with muscle loss in many medical conditions—including peripheral arterial disease, congestive heart failure, and COPD—that cause damage necessitating frequent regeneration, and exhaust the repairing capacity of resident satellite cells.”
From Age-related and disease-related muscle loss: The effect of diabetes, obesity, and other diseases (2014) · cites this paper as [109]
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Metadata
- Authors
- Buford, T. W., Anton, S. D., Judge, A. R., Marzetti, E., Wohlgemuth, S. E., Carter, C. S., Leeuwenburgh, C., Pahor, M., & Manini, T. M.
- Affiliations
- University of Florida (US)
- Corresponding author
- Buford, Thomas W.
- Manini, Todd M.
- ORCID
- Venue
- Ageing Research Reviews
- Publisher
- Elsevier BV
- Published
- 2010-10
- Volume
- 9
- Issue
- 4
- Pages
- 369-383
- ISSN
- 1568-1637 (ISSN-L)
- PMC
- PMC3788572
- OpenAlex
- W1967880601
- Cited by
- 295
- References
- 272
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 17 · 2023: 22 · 2022: 16 · 2021: 24 · 2020: 19 · 2019: 12 · 2018: 20 · 2017: 24 · 2016: 21 · 2015: 25 · 2014: 17 · 2013: 17 · 2012: 29
- FWCI
- 2.04
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Ageing Research Reviews (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (P30AG028740)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nutrition and Health in Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Keywords
- sarcopenia, age-related muscle loss, skeletal muscle, comorbidities, cancer, kidney disease, diabetes mellitus, peripheral arterial disease, nutrition, physical inactivity, therapeutic target
- MeSH terms
- Acceleration, Aged, Aged, 80 and over, Aging, Diabetes Mellitus, Feeding Behavior, Humans, Kidney Diseases, Health Knowledge, Attitudes, Practice, Models, Biological, Motor Activity, Neoplasms, Nutritional Requirements, Comorbidity, Apoptosis, Muscle, Skeletal, Sarcopenia, Peripheral Arterial Disease
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