Mitochondrial dysfunction in cellular senescence

Abstract

Cellular senescence is a complex biological process characterized by cell cycle arrest and the loss of a cell’s ability to divide. Despite the involvement of numerous molecular mechanisms, mitochondria play a central role in this process. Mitochondrial dysfunction, indicated by impaired respiratory capacity and a diminished energy status of the cell, is frequently accompanied by an augmented production of free oxygen radicals, resulting in oxidative stress. This condition not only accelerates cellular aging, but also its progression. A substantial body of research has substantiated the association between mitochondrial dysfunction and cellular senescence, underscoring the significance of mitochondria as a target for anti-aging therapies and interventions. The process of aging is associated with the onset of various age-related diseases, including cancer, cardiovascular diseases, and neurodegenerative diseases. A comprehensive understanding of these mechanisms offers novel opportunities to develop effective strategies that can mitigate the effects of senescence. This article summarizes the mechanisms contributing to the development of mitochondrial dysfunction during aging and discusses the main consequences of this impairment, particularly in the context of its impact on cellular senescence.