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Updated: Jun 27, 2026
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Preparation and Culture of Myogenic Precursor Cells/Primary Myoblasts from Skeletal Muscle of Adult and Aged Humans
Published on: February 16, 2017
Skeletal muscle proteolysis in aging.
Lydie Combaret1, Dominique Dardevet, Daniel Béchet
1INRA, Centre Clermont-Ferrand-Theix, UMR1019, Unité Nutrition Humaine, St. Genès Champanelle, France. combaret@clermont.inra.fr
Current Opinion in Clinical Nutrition and Metabolic Care
|December 6, 2008
Summary
Aging causes muscle loss (sarcopenia) due to impaired protein breakdown and increased cell death. Oxidative stress and mitochondrial issues worsen these age-related muscle changes.
Area of Science:
- Muscle physiology
- Cellular biology
- Aging research
Background:
- Sarcopenia, the age-related loss of muscle mass, results from an imbalance in protein synthesis and degradation.
- Cellular processes like apoptosis and regeneration are also implicated in sarcopenia.
- Understanding these mechanisms is crucial for addressing age-related muscle decline.
Purpose of the Study:
- To investigate age-related alterations in skeletal muscle proteolysis and apoptosis.
- To examine the role of oxidative stress and mitochondrial dysfunction in these changes.
- To elucidate the contributing factors to sarcopenia.
Main Methods:
- This review synthesizes current research on age-dependent changes in muscle proteolysis.
- It examines alterations in the ubiquitin-proteasome system and autophagy.
- Mitochondrial function and apoptosis pathways in aging muscle are analyzed.
Main Results:
- Aging impairs the ubiquitin-proteasome pathway's responsiveness to stimuli.
- Autophagy regulation is altered, and oxidative stress increases protein aggregation.
- Mitochondria-associated apoptosis pathways may be activated, contributing to sarcopenia.
Conclusions:
- Impaired proteolysis (proteasome and lysosomal pathways), increased oxidative stress, and mitochondrial dysfunction contribute to sarcopenia.
- These cellular changes reduce muscle function and the ability to recover from stress in older individuals.
- Targeting these pathways may offer strategies to mitigate age-related muscle loss.
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