Vascular endothelial senescence: from mechanisms to pathophysiology.
Most mitotically competent mammalian cell types can react to stress by undergoing a phenotypically distinctive and permanent form of growth arrest called "cellular senescence." This response has been extensively characterized in cell culture and more recently it has been found to occur also in vivo in a number of tissues. In this review I will present the case for the occurrence of senescence in the vascular endothelium. I will also discuss the mechanisms and factors that modulate endothelial cell replicative capacity and the onset of senescence. Finally, I will examine the senescent phenotype and its possible consequences for the development and progression of vascular diseases.
Erusalimsky
Jorge D
JD
Cardiff School of Health Sciences, University of Wales Institute, Cardiff CF5 2YB, UK. jderusalimsky@uwic.ac.uk
D000818:Animals; D017209:Apoptosis; D050197:Atherosclerosis / Q000473:pathology; D049109:Cell Proliferation; D016922:Cellular Senescence; D004249:DNA Damage; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D008928:Mitochondria / Q000473:pathology; D018919:Neovascularization, Physiologic; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D019098:Telomerase / Q000378:metabolism; D016615:Telomere / Q000378:metabolism; D013927:Thrombosis / Q000473:pathology; D014664:Vasodilation
D017382:Reactive Oxygen Species; D019098:Telomerase