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      Oxidative Stress, Mitochondrial Dysfunction, and Aging

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      Journal of Signal Transduction
      Hindawi Publishing Corporation

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          Abstract

          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.

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                Author and article information

                Journal
                J Signal Transduct
                JST
                Journal of Signal Transduction
                Hindawi Publishing Corporation
                2090-1739
                2090-1747
                2012
                2 October 2011
                : 2012
                : 646354
                Affiliations
                Department of Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655, USA
                Author notes

                Academic Editor: Paolo Pinton

                Article
                10.1155/2012/646354
                3184498
                21977319
                a79e51bb-0609-43f3-bbe2-0cff7f344897
                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.

                History
                : 15 May 2011
                : 3 August 2011
                Categories
                Review Article

                Cell biology
                Cell biology

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