Abstract
Age-related muscle atrophy is due to loss of muscle fibers as well as atrophy of the remaining fibers. Evidence shows that loss of myofibers may be, in part, due to apoptosis. Two major apoptotic pathways have been extensively studied which are the mitochondrion-mediated and receptor-mediated pathways. However, other pathways exist, such as the p53 pathway. To date, it is not completely clear what pathways are responsible for loss of fibers in age-related muscle atrophy. Evidence suggests that multiple pathways may play a role. In this review article the effects of aging on the mitochondrion-, receptor-, and p53-mediated apoptotic pathways in skeletal muscle are discussed.
Keywords: aging, sarcopenia, skeletal muscle, mitochondria, tumor necrosis factor alpha, p53, atrophy, muscle, DNA fragmentation
Current Aging Science
Title: Cellular and Molecular Mechanisms of Apoptosis in Age-Related Muscle Atrophy
Volume: 4 Issue: 3
Author(s): Amie J. Dirks-Naylor and Shannon Lennon-Edwards
Affiliation:
Keywords: aging, sarcopenia, skeletal muscle, mitochondria, tumor necrosis factor alpha, p53, atrophy, muscle, DNA fragmentation
Abstract: Age-related muscle atrophy is due to loss of muscle fibers as well as atrophy of the remaining fibers. Evidence shows that loss of myofibers may be, in part, due to apoptosis. Two major apoptotic pathways have been extensively studied which are the mitochondrion-mediated and receptor-mediated pathways. However, other pathways exist, such as the p53 pathway. To date, it is not completely clear what pathways are responsible for loss of fibers in age-related muscle atrophy. Evidence suggests that multiple pathways may play a role. In this review article the effects of aging on the mitochondrion-, receptor-, and p53-mediated apoptotic pathways in skeletal muscle are discussed.
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Cite this article as:
J. Dirks-Naylor Amie and Lennon-Edwards Shannon, Cellular and Molecular Mechanisms of Apoptosis in Age-Related Muscle Atrophy, Current Aging Science 2011; 4 (3) . https://dx.doi.org/10.2174/1874609811104030269
DOI https://dx.doi.org/10.2174/1874609811104030269 |
Print ISSN 1874-6098 |
Publisher Name Bentham Science Publisher |
Online ISSN 1874-6128 |
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