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Mechanisms of endothelial senescence
Author(s) -
Erusalimsky Jorge D.,
Skene Chris
Publication year - 2009
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2008.043133
Subject(s) - senescence , telomere , telomerase , oxidative stress , microbiology and biotechnology , biology , intracellular , endothelial stem cell , nitric oxide , cell , dna damage , genetics , in vitro , dna , endocrinology , gene
When endothelial cells from different vascular beds are grown in culture they show a limited capacity to divide, eventually entering into a permanent and phenotypically distinctive non‐dividing state referred to as ‘replicative senescence’. Replicative senescence is thought to result from progressive shortening of telomeric DNA and consequent telomere dysfunction. More recently, it has been realised that senescence can also be induced by a variety of insults, including those causing intracellular oxidative stress. In this report, we review evidence for the occurrence of endothelial cell senescence in vivo . We will also examine the causes, mechanisms and regulation of this process as they emerge from our studies in cell culture, focusing in particular on the roles of oxidative stress, telomerase, growth factors and nitric oxide.