Table of Contents
Journal of Signal Transduction
Volume 2012, Article ID 646354, 13 pages
Review Article

Oxidative Stress, Mitochondrial Dysfunction, and Aging

Department of Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655, USA

Received 15 May 2011; Accepted 3 August 2011

Academic Editor: Paolo Pinton

Copyright © 2012 Hang Cui 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.


Aging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases.