Mitochondrial abnormalities in muscle and other aging cells: Classification, causes, and effects
- 9 July 2002
- journal article
- review article
- Published by Wiley in Muscle & Nerve
- Vol. 26 (5) , 597-607
- https://doi.org/10.1002/mus.10194
Abstract
The involvement of mitochondria and of mitochondrial DNA (mtDNA) in the aging process has generated much interest and even more controversy. The mitochondrial theory of aging considers a vicious circle consisting of: (1) accumulation of somatic mtDNA mutations; (2) impairment of respiratory chain function; (3) increased production of reactive oxygen species (ROS) in mitochondria; and (4) further damage to mtDNA. We review the evidence for and against the belief that these steps occur in aging muscle and brain, considering separately morphological, biochemical, and molecular data. The relationship between mitochondrial aging and late‐onset neurodegenerative diseases is briefly reviewed. We conclude that mitochondrial dysfunction does play a crucial role in the aging process of both muscle and brain, but it remains unclear whether mitochondria are the culprits or mere accomplices. © 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 000–000,Keywords
This publication has 90 references indexed in Scilit:
- Mitochondrial enzyme activity in amyotrophic lateral sclerosis: Implications for the role of mitochondria in neuronal cell deathAnnals of Neurology, 1999
- Mitochondrial involvement in Alzheimer’s diseaseBiochimica et Biophysica Acta (BBA) - Bioenergetics, 1999
- Reduced Mitochondrial DNA Transcription in Senescent Rat HeartBiochemical and Biophysical Research Communications, 1998
- Role of mitochondrial DNA mutations in human aging: Implications for the central nervous system and muscleAnnals of Neurology, 1998
- Qualitative and Quantitative Changes in Skeletal Muscle mtDNA and Expression of Mitochondrial-Encoded Genes in the Human Aging ProcessBiochemical and Molecular Medicine, 1997
- Mitochondrial function in muscle from elderly athletesAnnals of Neurology, 1997
- Transfer of beta-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle.Proceedings of the National Academy of Sciences, 1996
- Aging, energy, and oxidative stress in neurodegenerative diseasesAnnals of Neurology, 1995
- Decline with age of the respiratory chain activity in human skeletal muscleBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 1994
- Age‐Dependent Impairment of Mitochondrial Function in Primate BrainJournal of Neurochemistry, 1993