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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References
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Journal ArticleDOI
Differential Regulation of Homocysteine Transport in Vascular Endothelial and Smooth Muscle Cells
Xiaohua Jiang,Fan Yang,Eugen Brailoiu,Hieronim Jakubowski,Nae J. Dun,Andrew I. Schafer,Xiao-feng Yang,Xiao-feng Yang,Xiao-feng Yang,William Durante,Hong Wang,Hong Wang,Hong Wang +12 more
TL;DR: The sodium-dependent system ASC predominantly mediates Hcy transport in EC and is lysosomal dependent, while the large branched-chain neutral amino acids (L) transporter systems in HAECs and ASC>L>XAG in HASMCs play a predominant role in vascular cells.
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Protective effect of melatonin against homocysteine-induced vasoconstriction of human umbilical artery.
TL;DR: It is suggested that Hcy potentiates vascular tension in human umbilical artery, possibly by suppressing bioavailable NO and protecting against the vasoconstrictive effect of Hcy, most likely by scavenging (*)OH arising from Hcy autooxidation.
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Moderate Hyperhomocysteinemia Decreases Endothelial-Dependent Vasorelaxation in Pregnant But Not Nonpregnant Mice
TL;DR: In pregnant mice, endothelial-dependent vasodilation is more sensitive to the effect of increased homocysteine than arteries from nonpregnant mice, which appears to result from a loss in NO-mediated relaxation that may be mediated by the oxidative inactivation of the NO synthase cofactor tetrahydrobiopterin.
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Tetrahydrobiopterin attenuates homocysteine induced endothelial dysfunction.
TL;DR: Hyperhomocysteine impairs endothelial function, in part due to a diminished bioavailability of BH4 with resultant uncoupling of nitric oxide synthase, and may represent an important target for strategies aimed at improving endothelial dysfunction secondary to hyperhomocysteinemia.
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Homocysteine-induced endothelin-1 release is dependent on hyperglycaemia and reactive oxygen species production in bovine aortic endothelial cells.
TL;DR: The combined metabolic burden of Hcy and high glucose stimulates ET-1 synthesis in bovine aortic endothelial cells via a mechanism dependent on the production of mitochondrial ROS, but may not be generalisable to all types of endothelial Cells.