Mitochondrial function and myocardial aging. A critical analysis of the role of permeability transition

Mitochondria have been suggested to be causally linked to age-related alterations through respiratory chain dysfunction and formation of reactive oxygen species, leading to damage of mitochondrial DNA. Impaired biosynthesis of respiratory chain and ATP synthase subunits encoded by mitochondrial gene...

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Bibliographic Details
Published in:Cardiovascular research 2005-05, Vol.66 (2), p.222-232
Main Authors: DI LISA, Fabio, BERNARDI, Paolo
Format: Article
Language:English
Subjects:
Aging - physiology
Biological and medical sciences
Calcium - metabolism
Cardiology. Vascular system
Cell Death
Cell Respiration
DNA Damage
DNA, Mitochondrial
Electron Transport
Humans
Ion Channels - physiology
Medical sciences
Mitochondria, Heart - physiology
Mitochondrial ADP, ATP Translocases - metabolism
Mitochondrial Membrane Transport Proteins
Myocardial Ischemia - metabolism
Myocardial Ischemia - pathology
Oxidative Stress
Reactive Oxygen Species - metabolism
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Summary:Mitochondria have been suggested to be causally linked to age-related alterations through respiratory chain dysfunction and formation of reactive oxygen species, leading to damage of mitochondrial DNA. Impaired biosynthesis of respiratory chain and ATP synthase subunits encoded by mitochondrial genes would set up a vicious cycle contributing to the aging process. Mitochondria are also involved in the increased susceptibility to ischemic injury observed in aged hearts, a process where the mitochondrial permeability transition pore (PTP) may play a role. Here, we analyze (i) the possible mechanisms through which PTP opening might contribute to age-related myocardial alterations; (ii) the available evidence of an increased probability of PTP opening in mitochondria isolated from aged tissues; (iii) the current methodological limitations that complicate the elucidation of causal relationships between PTP opening, mitochondrial dysfunction, and myocardial aging.
ISSN:0008-6363
1755-3245
DOI:10.1016/j.cardiores.2005.02.009