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Cellular and molecular mechanisms of apoptosis in age-related muscle atrophy

Amie J Dirks-Naylor1, Shannon Lennon-Edwards

  • 1School of Pharmacy, Wingate University, Wingate, NC 28174, USA. anaylor@wingate.edu

Current Aging Science
|May 3, 2011
PubMed

Insights

Aging causes skeletal muscle atrophy through the loss of muscle fibers, potentially via apoptosis. This review examines the roles of mitochondrion-, receptor-, and p53-mediated apoptotic pathways in age-related muscle fiber loss.

Area of Science:

  • Gerontology
  • Cell Biology
  • Skeletal Muscle Physiology

Background:

  • Age-related muscle atrophy, or sarcopenia, involves myofiber loss and shrinkage.
  • Apoptosis (programmed cell death) is implicated in myofiber loss during aging.
  • Mitochondrion-mediated and receptor-mediated pathways are known apoptosis routes, but others like the p53 pathway also exist.

Purpose of the Study:

  • To review the impact of aging on key apoptotic pathways in skeletal muscle.
  • To elucidate the specific roles of mitochondrion-, receptor-, and p53-mediated apoptosis in age-related muscle atrophy.

Main Methods:

  • Literature review of studies on aging, skeletal muscle, and apoptosis.
  • Analysis of research investigating mitochondrion-, receptor-, and p53-mediated cell death pathways.
  • Synthesis of evidence regarding the contribution of these pathways to sarcopenia.

Main Results:

  • Aging affects multiple apoptotic pathways in skeletal muscle.
  • The precise contribution of each pathway (mitochondrion-, receptor-, p53-mediated) to age-related muscle fiber loss is still under investigation.
  • Evidence suggests a complex interplay between different apoptotic mechanisms.

Conclusions:

  • Multiple apoptotic pathways likely contribute to skeletal muscle atrophy during aging.
  • Further research is needed to fully understand the mechanisms driving age-related myofiber loss.
  • Targeting specific apoptotic pathways may offer therapeutic strategies for sarcopenia.

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