Hyperhomocysteinemia and Endothelial Dysfunction.
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TLDR
Six mechanisms have been suggested explaining HHcy-induced endothelial dysfunction and the goal of this review is to elaborate these mechanisms and to discuss biological and molecular events related to HHCy-induced ED.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.read more
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Homocysteine inhibits endothelial progenitor cells proliferation via DNMT1-mediated hypomethylation of Cyclin A.
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References
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Journal Article
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Jonathan S. Stamler,John A. Osborne,Omar Jaraki,LeRoy E. Rabbani,Mark E. Mullins,David J. Singel,Joseph Loscalzo +6 more
TL;DR: These results suggest that the normal endothelium modulates the potential, adverse effects of homocysteine by releasing EDRF and forming the adduct S-NO-homocysteines, a potent antiplatelet agent and vasodilator.
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EDHF: bringing the concepts together.
TL;DR: Several mechanisms have been proposed to link this pivotal step to the subsequent smooth muscle hyperpolarization and the main concepts are considered in detail in this review.
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Homocysteine Impairs the Nitric Oxide Synthase Pathway Role of Asymmetric Dimethylarginine
Markus Stühlinger,Philip S. Tsao,Jeng Horng Her,Masumi Kimoto,Robert F. Balint,John P. Cooke +5 more
TL;DR: Homocysteine post-translationally inhibits DDAH enzyme activity, causing ADMA to accumulate and inhibit nitric oxide synthesis, which may explain the known effect of homocysteines to impair endothelium-mediated nitricoxide–dependent vasodilatation.