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Modulation of cell death in age-related diseases

Tugsan Tezil, Huveyda Basaga1

  • 1Biological Sciences and Bioengineering Program, Sabanci University, 34956, Tuzla, Istanbul, Turkey. huveyda@sabanciuniv.edu.

Current Pharmaceutical Design
|October 2, 2013
PubMed

Insights

Aging is linked to cellular damage from reactive oxygen species (ROS). This review explores how oxidative stress and disrupted cell death (apoptosis and autophagy) signaling contribute to aging and diseases.

Area of Science:

  • Cellular Biology
  • Gerontology
  • Biochemistry

Background:

  • Aging is a universal biological process.
  • The free-radical theory posits that accumulated reactive oxygen species (ROS) damage cells, impairing homeostasis.
  • This damage can lead to cellular dysfunction and age-related pathologies.

Purpose of the Study:

  • To review current understanding of oxidative stress in aging.
  • To examine the dysregulation of cell death signaling pathways during aging.
  • To explore the link between these processes and age-related diseases.

Main Methods:

  • Literature review of studies on oxidative stress and aging.
  • Analysis of research on apoptosis and autophagy signaling.
  • Synthesis of hypotheses on age-related cellular damage and death pathways.

Main Results:

  • Oxidative stress from ROS causes DNA, protein, and lipid damage.
  • Impaired antioxidant defenses lead to accumulated molecular damage.
  • Dysregulation of programmed cell death (apoptosis and autophagy) is implicated in aging.

Conclusions:

  • Oxidative stress is a key factor in cellular aging.
  • Altered cell death pathways contribute to age-related diseases like cancer and neurodegenerative disorders.
  • Further research into these pathways may reveal therapeutic targets for aging.

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