4.6 Review

Is there more to aging than mitochondrial DNA and reactive oxygen species?

Journal

FEBS JOURNAL
Volume 276, Issue 20, Pages 5768-5787

Publisher

WILEY
DOI: 10.1111/j.1742-4658.2009.07269.x

Keywords

antioxidants; lifespan extension; mitochondria; mitochondrial DNA degradation; mitochondrial DNA mutations; mitochondrial DNA repair; mitochondrial theory of aging; oxidative damage

Funding

  1. National Institutes of Health [P01 HL06629907, R21RR02396101]
  2. NATIONAL CENTER FOR RESEARCH RESOURCES [R21RR023961, R01RR031286] Funding Source: NIH RePORTER
  3. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL066299] Funding Source: NIH RePORTER
  4. OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [R01OD010944] Funding Source: NIH RePORTER

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With the aging of the population, we are seeing a global increase in the prevalence of age-related disorders, especially in developed countries. Chronic diseases disproportionately affect the older segment of the population, contributing to disability, a diminished quality of life and an increase in healthcare costs. Increased life expectancy reflects the success of contemporary medicine, which must now respond to the challenges created by this achievement, including the growing burden of chronic illnesses, injuries and disabilities. A well-developed theoretical framework is required to understand the molecular basis of aging. Such a framework is a prerequisite for the development of clinical interventions that will constitute an efficient response to the challenge of age-related health issues. This review critically analyzes the experimental evidence that supports and refutes the Free Radical/Mitochondrial Theory of Aging, which has dominated the field of aging research for almost half a century.

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