Vascular endothelial senescence: from mechanisms to pathophysiology

被引:326
作者
Erusalimsky, Jorge D. [1 ]
机构
[1] UWIC, Cardiff Sch Hlth Sci, Cardiff CF5 2YB, S Glam, Wales
关键词
endothelium; oxidative stress; telomere; REGULATES TELOMERASE ACTIVITY; PROGENITOR-CELL SENESCENCE; PLASMINOGEN-ACTIVATOR INHIBITOR; INDUCED PREMATURE SENESCENCE; FIBROBLAST GROWTH FACTOR-2; NITRIC-OXIDE; OXIDATIVE STRESS; IN-VITRO; REPLICATIVE SENESCENCE; CARDIOVASCULAR-DISEASE;
D O I
10.1152/japplphysiol.91353.2008
中图分类号
Q4 [生理学];
学科分类号
071003 [生理学];
摘要
Erusalimsky JD. Vascular endothelial senescence: from mechanisms to pathophysiology. J Appl Physiol 106: 326-332, 2009; doi:10.1152/japplphysiol.91353.2008.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.
引用
收藏
页码:326 / 332
页数:7
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