Journal
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS
Volume 1847, Issue 11, Pages 1347-1353Publisher
ELSEVIER
DOI: 10.1016/j.bbabio.2015.05.022
Keywords
DNA; Mitochondrial; Aging
Categories
Funding
- Academy of Medical Sciences
- Wellcome Trust [101876/Z/13/Z, 096919Z/11/Z]
- Medical Research Council
- British Heart Foundation
- Arthritis Research UK
- Prostate Cancer UK
- Royal College of Physicians
- Medical Research Council (UK) Centre for Translational Muscle Disease research [G0601943]
- EU FP7 TIRCON
- National Institute for Health Research (NIHR), Newcastle Biomedical Research Centre based at Newcastle upon Tyne Hospitals NHS Foundation Trust and Newcastle University
- Academy of Medical Sciences (AMS) [AMS-SGCL12-Payne] Funding Source: researchfish
- Medical Research Council [G0800470, G0601943] Funding Source: researchfish
- National Institute for Health Research [CL-2013-01-004] Funding Source: researchfish
- MRC [G0800470, G0601943] Funding Source: UKRI
- Wellcome Trust [101876/Z/13/Z] Funding Source: Wellcome Trust
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The free radical theory of aging is almost 60 years old. As mitochondria are the principle source of intracellular reactive oxygen species (ROS), this hypothesis suggested a central role for the mitochondrion in normal mammalian aging. In recent years, however, much work has questioned the importance of mitochondrial ROS in driving aging. Conversely new evidence points to other facets of mitochondrial dysfunction which may nevertheless suggest the mitochondrion retains a critical role at the center of a complex web of processes leading to cellular and organismal aging. Crown Copyright (c) 2015 Published by Elsevier B.V.
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