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Published in: Longevity & Healthspan 1/2014

Open Access 01-12-2014 | Review

Mitochondrial oxidative stress in aging and healthspan

Authors: Dao-Fu Dai, Ying Ann Chiao, David J Marcinek, Hazel H Szeto, Peter S Rabinovitch

Published in: Longevity & Healthspan | Issue 1/2014

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Abstract

The free radical theory of aging proposes that reactive oxygen species (ROS)-induced accumulation of damage to cellular macromolecules is a primary driving force of aging and a major determinant of lifespan. Although this theory is one of the most popular explanations for the cause of aging, several experimental rodent models of antioxidant manipulation have failed to affect lifespan. Moreover, antioxidant supplementation clinical trials have been largely disappointing. The mitochondrial theory of aging specifies more particularly that mitochondria are both the primary sources of ROS and the primary targets of ROS damage. In addition to effects on lifespan and aging, mitochondrial ROS have been shown to play a central role in healthspan of many vital organ systems. In this article we review the evidence supporting the role of mitochondrial oxidative stress, mitochondrial damage and dysfunction in aging and healthspan, including cardiac aging, age-dependent cardiovascular diseases, skeletal muscle aging, neurodegenerative diseases, insulin resistance and diabetes as well as age-related cancers. The crosstalk of mitochondrial ROS, redox, and other cellular signaling is briefly presented. Potential therapeutic strategies to improve mitochondrial function in aging and healthspan are reviewed, with a focus on mitochondrial protective drugs, such as the mitochondrial antioxidants MitoQ, SkQ1, and the mitochondrial protective peptide SS-31.
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Metadata
Title
Mitochondrial oxidative stress in aging and healthspan
Authors
Dao-Fu Dai
Ying Ann Chiao
David J Marcinek
Hazel H Szeto
Peter S Rabinovitch
Publication date
01-12-2014
Publisher
BioMed Central
Published in
Longevity & Healthspan / Issue 1/2014
Electronic ISSN: 2046-2395
DOI
https://doi.org/10.1186/2046-2395-3-6

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