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BioMed Research International
Volume 2014, Article ID 238463, 7 pages
http://dx.doi.org/10.1155/2014/238463
Review Article

Mitochondrial Aging and Age-Related Dysfunction of Mitochondria

1Department of Medical Nanobiotechnology, Pirogov Russian State Medical University, Moscow 117997, Russia
2Laboratory of Medical Genetics, Russian Cardiology Research and Production Complex, Moscow 121552, Russia
3Laboratory of Cellular Mechanisms of Atherogenesis, Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow 125315, Russia
4Biological Faculty, N.P. Ogaryov Mordovian State University, Saransk 430005, Russia
5Institute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow 143025, Russia
6Faculty of Medicine, University of New South Wales, Sydney, NSW 2052, Australia
7School of Medicine, University of Western Sydney, Campbelltown, NSW 2560, Australia

Received 16 December 2013; Accepted 19 March 2014; Published 10 April 2014

Academic Editor: Ancha Baranova

Copyright © 2014 Dimitry A. Chistiakov et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Age-related changes in mitochondria are associated with decline in mitochondrial function. With advanced age, mitochondrial DNA volume, integrity and functionality decrease due to accumulation of mutations and oxidative damage induced by reactive oxygen species (ROS). In aged subjects, mitochondria are characterized by impaired function such as lowered oxidative capacity, reduced oxidative phosphorylation, decreased ATP production, significant increase in ROS generation, and diminished antioxidant defense. Mitochondrial biogenesis declines with age due to alterations in mitochondrial dynamics and inhibition of mitophagy, an autophagy process that removes dysfunctional mitochondria. Age-dependent abnormalities in mitochondrial quality control further weaken and impair mitochondrial function. In aged tissues, enhanced mitochondria-mediated apoptosis contributes to an increase in the percentage of apoptotic cells. However, implementation of strategies such as caloric restriction and regular physical training may delay mitochondrial aging and attenuate the age-related phenotype in humans.