Endothelial aging.
Aging is considered to be the major risk factor for the development of atherosclerosis and, therefore, for coronary artery disease. Apart from age-associated remodeling of the vascular wall, which includes luminal enlargement, intimal and medial thickening, and increased vascular stiffness, endothelial function declines with age. This is most obvious from the attenuation of endothelium-dependent dilator responses, which is a consequence of the alteration in the expression and/or activity of the endothelial NO synthase, upregulation of the inducible NO synthase, and increased formation of reactive oxygen species. Aging is also associated with a reduction in the regenerative capacity of the endothelium and endothelial senescence, which is characterized by an increased rate of endothelial cell apoptosis.
Brandes
Ralf P
RP
Institut für Kardiovaskuläre Physiologie, J.W. Goethe-Universität, Theodor-Stern-Kai 7, D-60596 Frankfurt am Main, Germany. r.brandes@em.uni-frankfurt.de
Fleming
Ingrid
I
Busse
Rudi
R
D000368:Aged; D000375:Aging / Q000502:physiology*; D017209:Apoptosis; D016922:Cellular Senescence; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D014664:Vasodilation / Q000502:physiology
D017382:Reactive Oxygen Species; C496319:NOS2 protein, human; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III