Oxidative stress response elicited by mitochondrial dysfunction: implication in the pathophysiology of aging

Oxidative stress response elicited by mitochondrial dysfunction: implication in the pathophysiology of aging


Mitochondrial reactive oxygen species (ROS) accumulation is thought to participate in a vicious cycle of oxidative damage in aging. Damaged mtDNA results in a faulty respiratory chain, causing ROS generation, which may further damage the mtDNA, and so on. In this review, the authors discuss some of the mechanisms of mitochondrial dysfunction in aging, and potential ways this may be regulated. In particular, calorie restriction has been observed to reduce age-related phenotypes. The authors present evidence supporting the claim that a family of deacetylases called sirtuins, which commonly modify mitochondrial proteins, are responsible for this. The authors also discuss how low-levels of ROS are important for autophagic signalling, a pro-cell survival response which recycles damaged organelles. Loss of this quality control has been shown in aging and aging-related disorders such as neurodegenerative diseases.