Mitochondria: Potential Targets for Interventions to Counteract Senescence

Abstract

Cellular senescence, an irreversible cell-cycle arrest, has been shown to occur in a variety of physiological contexts and play multiple functions. Importantly, recent data indicates that senescence is not only associated with aging and age-related diseases, but also plays a causal role in these processes. Senescence is thought to contribute to tissue dysfunction mostly through the generation of a senescence associated secretory phenotype (SASP) which can induce chronic inflammation, changes in tissue architecture, stem cell depletion and spread senescence in otherwise young healthy cells. An important feature of cellular senescence is mitochondrial dysfunction, which has been shown not only to contribute to the cell-cycle arrest but also to tightly regulate the SASP. In this book chapter, we review some of the most up-to-date literature on the role of mitochondria during cellular senescence. Finally, we propose that by targeting mitochondria we may be able to counteract the detrimental effects of cellular senescence during aging and associated diseases.