Abstract
SummaryThe cellular mechanisms responsible for aging are poorly understood. Aging is considered as a degenerative process induced by the accumulation of cellular lesions leading progressively to organ dysfunction and death. The free radical theory of aging has long been considered the most relevant to explain the mechanisms of aging. As the mitochondrion is an important source of reactive oxygen species (ROS), this organelle is regarded as a key intracellular player in this process and a large amount of data supports the role of mitochondrial ROS production during aging. Thus, mitochondrial ROS, oxidative damage, aging, and aging‐dependent diseases are strongly connected. However, other features of mitochondrial physiology and dysfunction have been recently implicated in the development of the aging process. Here, we examine the potential role of the mitochondrial permeability transition pore (mPTP) in normal aging and in aging‐associated diseases.
Highlights
Aging is a physiological process occurring over life that induces a general decline of physical and mental capacities
The aim of this review is to summarize the current data showing a relationship between mitochondrial permeability transition pore (mPTP) opening and aging
It is essential to understand the cellular mechanism of aging to improve the quality of life of the elderly and to apply strategies to fight against the pathologies appearing during aging
Summary
Aging is a physiological process occurring over life that induces a general decline of physical and mental capacities. It is likely that the mechanisms described in these theories may participate to those of aging but none of them can directly explain the causes of aging Another theory centered on mitochondrial dysfunction was proposed half a century ago (Harman, 1972). One of the unique characteristics of mitochondria is that they possess their own genetic material in the form of a close circular DNA molecule According to this latter theory, aging of cells would be due to the constant delivery of ROS inside mitochondria throughout life, damaging mitochondrial DNA which is vulnerable as it is not protected by protein histones or repairing enzymes such as nuclear DNA. The damaged mitochondrial DNA leads to deficiency of key electron transport enzymes and subsequent ROS generation, causing a vicious cycle of ROS resulting in a decrease in energy production (Fariss, Chan, Patel, Van Houten, & Orrenius, 2005)
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