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Programmed cell death in aging

John Tower1

  • 1Molecular and Computational Biology Program, Department of Biological Sciences, University of Southern California, 1050 Childs Way, RRI 201, Los Angeles, CA 90089-2910, USA.

Ageing Research Reviews
|April 12, 2015
PubMed

Insights

Programmed cell death (PCD) pathways are crucial for tissue health but become dysregulated during aging. This imbalance contributes to age-related diseases and affects cell turnover, impacting longevity.

Area of Science:

  • Cell Biology
  • Aging Research
  • Physiology

Background:

  • Programmed cell death (PCD) pathways, encompassing apoptosis and regulated necrosis, are vital for cellular turnover and maintaining tissue homeostasis.
  • Dysregulation of PCD is increasingly linked to the aging process and age-related diseases.
  • Aging is characterized by declining cell turnover in highly proliferative tissues.

Purpose of the Study:

  • To explore the role of programmed cell death (PCD) in aging.
  • To understand how aging-associated disruptions impact PCD pathways.
  • To investigate the implications of altered PCD in age-related conditions.

Main Methods:

  • Review of existing literature on PCD and aging.
  • Analysis of cellular and systemic signaling changes during aging.
  • Examination of mitochondrial function in relation to PCD.

Main Results:

  • Aging leads to altered PCD rates, with increased rates in some cells and decreased rates in others.
  • Increased PCD contributes to immune decline, sarcopenia, cardiac cell loss, and neurodegeneration.
  • Cancer and senescent cells exhibit resistance to PCD, promoting their accumulation with age.

Conclusions:

  • Mitochondrial malfunction and signaling disruptions are key factors in aging-associated PCD dysregulation.
  • Altered PCD pathways have significant implications for age-related pathologies and tissue function.
  • The precise role of PCD in limiting adult metazoan lifespan requires further investigation.
Keywords:
AgingApoptosisMitochondriaNecrosisSarcopeniaSenescence

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