Stress-induced premature senescence of endothelial cells: a perilous state between recovery and point of no return

Abstract

To discuss most recently published studies on morphologic patterns and molecular mechanisms of stress-induced premature senescence (SIPS) of vascular endothelial cells. Lysosomal dysfunction and impaired autophagy, which have been well established in replicative senescence, were also described in SIPS induced by advanced glycation end products (AGEs). Recently, strides were made to prevent and reverse senescence. The role of lysosomal dysfunction and Lamp-2A deficiency has been demonstrated in aging. Molecular analyses identified the role of sirtuin 1 in preventing cell senescence; shed light on the role of polycomb group (PcG) protein Bmi-1 in senescence. Additionally, intriguing data on the role of caveolin-1 in cell senescence have emerged. In aging organisms and chronic diseases properly functioning tissue is replaced by senescent cells. Comparison between replicative senescence and SIPS indicates that replicative senescence is almost exclusively associated with the reduction of telomerase activity and attrition of telomeres, whereas SIPS does not require these events, thus conferring potential reversibility onto this process.