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Journal of Aging Research
Volume 2011 (2011), Article ID 810619, 12 pages
Review Article

Mitochondria and PGC-1α in Aging and Age-Associated Diseases

Institute for Genetics, Cluster of Excellence, Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Straße 47A, 50674 Cologne, Germany

Received 15 October 2010; Revised 23 February 2011; Accepted 24 February 2011

Academic Editor: Reinald Pamplona

Copyright © 2011 Tina Wenz. 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 the most significant risk factor for a range of degenerative disease such as cardiovascular, neurodegenerative and metabolic disorders. While the cause of aging and its associated diseases is multifactorial, mitochondrial dysfunction has been implicated in the aging process and the onset and progression of age-associated disorders. Recent studies indicate that maintenance of mitochondrial function is beneficial in the prevention or delay of age-associated diseases. A central molecule seems to be the peroxisome proliferator-activated receptor γ coactivator α (PGC-1α), which is the key regulator of mitochondrial biogenesis. Besides regulating mitochondrial function, PGC-1α targets several other cellular processes and thereby influences cell fate on multiple levels. This paper discusses how mitochondrial function and PGC-1α are affected in age-associated diseases and how modulation of PGC-1α might offer a therapeutic potential for age-related pathology.