Mitochondrial responsibility in ageing process: innocent, suspect or guilty.
Guillermo López-Lluch1, Carlos Santos-Ocaña, José Antonio Sánchez-Alcázar
1Centro Andaluz de Biología del Desarrollo, CABD-CSIC, CIBERER, Instituto Carlos III, Universidad Pablo de Olavide, Carretera de Utrera km. 1, 41013, Seville, Spain, glopllu@upo.es.
Biogerontology
|June 25, 2015
Summary
Mitochondrial dysfunction is central to aging, impacting cellular health and metabolism. Interventions targeting mitochondria may extend lifespan and healthspan by enhancing biogenesis and mitophagy.
Area of Science:
- Gerontology
- Cell Biology
- Mitochondrial Biology
Background:
- Cellular damage from stressors, including reactive oxygen species (ROS), accumulates with age.
- Mitochondrial dysfunction, affecting electron transport chain, biogenesis, turnover, and apoptosis, is increasingly recognized as a key factor in aging.
- Mitochondria play a crucial role in cellular metabolism and ROS production, influencing organismal aging.
Purpose of the Study:
- To review the central role of mitochondria in the aging process across various model organisms.
- To discuss whether mitochondrial dysfunction is a cause or consequence of aging.
- To highlight potential therapeutic targets within mitochondria for extending healthspan.
Main Methods:
- Review of existing literature on aging and mitochondrial function.
- Analysis of studies across diverse model organisms (yeast, worm, fruit fly, mice).
- Discussion of the interplay between mitochondrial health and aging phenotypes.
Main Results:
- Mitochondrial dysfunction is implicated in various aging phenotypes.
- Interventions like caloric restriction, exercise, and plant-derived compounds can modulate mitochondrial activity (biogenesis, mitophagy).
- Mitochondria are central to metabolic regulation relevant to aging.
Conclusions:
- Mitochondria are critical determinants of aging, influencing lifespan and healthspan.
- Targeting mitochondrial pathways offers potential for anti-aging interventions.
- Further research is needed to elucidate the causal relationship between mitochondrial dysfunction and aging.
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