Hyperhomocysteinemia and Endothelial Dysfunction

Title: Hyperhomocysteinemia and Endothelial Dysfunction

Volume: 5 Issue: 2

Author(s): Zhong-Jian Cheng, Xiaofeng Yang and Hong Wang

Affiliation:

Keywords: Hyperhomocysteinemia, endothelial dysfunction, vascular relaxation/vascular contractile responses

Abstract: 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.

Cite this article as:

Cheng Zhong-Jian, Yang Xiaofeng and Wang Hong, Hyperhomocysteinemia and Endothelial Dysfunction, Current Hypertension Reviews 2009; 5 (2) . https://dx.doi.org/10.2174/157340209788166940