Senescence and its bypass in the vascular endothelium.
Vascular endothelial cells line the interior of blood vessels. As in other cell types, the proliferative lifespan of endothelial cells is limited; after a given number of replication cycles, they undergo senescence. Angiogenesis, the formation of new capillaries from pre-existing vasculature, is a process that involves endothelial cell proliferation. Angiogenesis thus has the possibility to be limited by the occurrence of senescence in the endothelial cell population. While there is evidence that endothelial cells undergo senescence in vivo, there are also data implying that endothelial senescence can be delayed or prevented in certain situations. Such a prevention of senescence would allow continued endothelial cell proliferation and continued angiogenesis in both physiological and pathological settings. This review discusses endothelial cell senescence and its bypass in vitro and in vivo.
Freedman
Deborah Anne
DA
Vascular Biology Program, Department of Surgery, Children's Hospital, Harvard Medical School, 1 Blackfan Circle, Boston, MA 02115, USA. Deborah.freedman@childrens.harvard.edu <Deborah.freedman@childrens.harvard.edu>
D000818:Animals; D050197:Atherosclerosis / Q000473:pathology; D018929:Cell Culture Techniques; D045744:Cell Line, Tumor; D016922:Cellular Senescence; D018844:Cyclin-Dependent Kinases / Q000037:antagonists & inhibitors; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D009369:Neoplasms / Q000473:pathology; D009389:Neovascularization, Pathologic; D016615:Telomere / Q000648:ultrastructure; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014945:Wound Healing
D016159:Tumor Suppressor Protein p53; D018844:Cyclin-Dependent Kinases