Hyperhomocysteinemia and endothelial dysfunction
Hyperhomocysteinemia (HHcy) is a significant and independent risk factor for
cardiovascular diseases. Endothelial dysfunction (ED) is the earliest indicator of
atherosclerosis and vascular diseases. We and others have shown that HHcy induced ED in
human and in animal models of HHcy induced by either high-methionine load or genetic
deficiency. Six mechanisms have been suggested explaining HHcy-induced ED. These
include 1) nitric oxide inhibition, 2) prostanoids regulation, 3) endothelium-derived …
cardiovascular diseases. Endothelial dysfunction (ED) is the earliest indicator of
atherosclerosis and vascular diseases. We and others have shown that HHcy induced ED in
human and in animal models of HHcy induced by either high-methionine load or genetic
deficiency. Six mechanisms have been suggested explaining HHcy-induced ED. These
include 1) nitric oxide inhibition, 2) prostanoids regulation, 3) endothelium-derived …
Hyperhomocysteinemia (HHcy) is a significant and independent risk factor for cardiovascular diseases. Endothelial dysfunction (ED) is the earliest indicator of atherosclerosis and vascular diseases. We and others have shown that HHcy induced ED in human and in animal models of HHcy induced by either high-methionine load or genetic deficiency. Six mechanisms have been suggested explaining HHcy-induced ED. These include 1) nitric oxide inhibition, 2) prostanoids regulation, 3) endothelium-derived hyperpolarizing factors suppression, 4) angiotensin II receptor-1 activation, 5) endothelin-1 induction, and 6) oxidative stress. The goal of this review is to elaborate these mechanisms and to discuss biological and molecular events related to HHcy-induced ED.
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