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- W2160444804 endingPage "H1739" @default.
- W2160444804 startingPage "H1729" @default.
- W2160444804 abstract "Senescence has been considered a programmed cellular response, parallel to apoptosis, that is turned on when a cell reaches Hayflick's limit. Once cells enter the senescence program, they cease to proliferate and undergo a series of morphological and functional changes. Studies support a central role for Rb protein in controlling this process after it receives senescent signals from the p53 and p16 pathways. Cellular senescence is considered an essential contributor to the aging process and has been shown to be an important tumor suppression mechanism. In addition, emerging evidence suggests that senescence may also be involved in the pathogenesis of stem cell dysfunction and chronic human diseases. Under these circumstances cells undergo stress-induced premature senecence, which has several specific features. Focusing on endothelial cells, we discuss recent advances in our understanding of the stresses and their pathways that prompt the premature senescence response, evaluate their correlation with the apoptotic response, and examine their links to the development of chronic diseases and the impaired function of endothelial progenitor cells, with the emphasis on vasculopathy. Emerging novel therapeutic interventions based on recent experimental findings are also reviewed." @default.
- W2160444804 created "2016-06-24" @default.
- W2160444804 creator A5050906977 @default.
- W2160444804 creator A5082857859 @default.
- W2160444804 date "2006-05-01" @default.
- W2160444804 modified "2023-10-16" @default.
- W2160444804 title "Premature senescence of endothelial cells: Methusaleh's dilemma" @default.
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