Fig. 3

ROS as a driver of senescence. Enhanced ROS levels result in cellular damage and consequent cell cycle arrest mediated via p53, p21, and p16. Moreover, ROS damages mitochondrial DNA (mtDNA) and causes lipid peroxidation initiating mitochondrial dysfunction and thus lead to enhanced ROS generation. Other senescence features are the expression of senescence-associated β-galactosidase (SA-β-Gal), downregulation of Sirt1 and Sirt6, upregulation of p21 and p16, presence of enlarged mitochondria, inhibition of mitophagy, and secretion of senescence-associated secretory phenotype (SASP) factors mainly driven by the NFκB