Review
Copyright ©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Exp Med. Nov 20, 2014; 4(4): 46-57
Published online Nov 20, 2014. doi: 10.5493/wjem.v4.i4.46
Aging: A mitochondrial DNA perspective, critical analysis and an update
Inna N Shokolenko, Glenn L Wilson, Mikhail F Alexeyev
Inna N Shokolenko, Biomedical Sciences Department, Patt Capps Covey College of Allied Health Professions, University of South Alabama, Mobile, AL 36688-0002, United States
Glenn L Wilson, Mikhail F Alexeyev, Department of Cell Biology and Neuroscience, University of South Alabama, Mobile, AL 36688, United States
Mikhail F Alexeyev, Pharmacology and Center for Lung Biology, University of South Alabama, Mobile, AL 36688, United States
Author contributions: Shokolenko IN and Alexeyev MF conceived the manuscript, collected the literature, wrote, edited and revised the manuscript; Wilson GL conceived the manuscript, edited and revised the manuscript.
Supported by The National Institutes of Health grants No. ES03456, PO1 HL66299, and No. OD010944
Correspondence to: Mikhail F Alexeyev, PhD, Department of Cell Biology and Neuroscience, University of South Alabama, 5851 USA Dr. North, MSB1201, Mobile, AL 36688, United States. malexeye@southalabama.edu
Telephone: +1-251-4606789 Fax: +1-251-4606771
Received: May 27, 2014
Revised: July 15, 2014
Accepted: August 27, 2014
Published online: November 20, 2014
Processing time: 176 Days and 8.6 Hours
Core Tip

Core tip: The notion of reactive oxygen species (ROS) -mediated accumulation of mutations in mitochondrial DNA (mtDNA) as a driving force behind aging is increasingly losing ground forcing a revision of the Mitochondrial Theory of Aging. While mitochondrial involvement remains in the center of attention of aging research, the focus is shifting from mtDNA mutations to mitochondrial physiology. The positive effect of increased ROS production on longevity is increasingly viewed as evidence that increased ROS production in aging may be adaptive rather than maladaptive. This novel paradigm explains failure of antioxidants to delay aging in clinical trials.