Homocysteine-Induced Endothelial Dysfunction

This review discussed and in particular emphasis the potential cellular pathways and the biological processes involved that lead to homocysteine-induced endothelial dysfunction, in particular in the impaired endothelial dependent dilatation aspect. Hyperhomocysteinemia is an independent cardiovascul...

Full description

Saved in:
Bibliographic Details
Published in:Annals of nutrition and metabolism 2015-01, Vol.67 (1), p.1-12
Main Authors: Lai, Wai Keung Christopher, Kan, Ming Yin
Format: Article
Language:English
Subjects:
Bioavailability
Biological Availability
Biology
Cardiovascular Diseases - etiology
Cardiovascular Diseases - physiopathology
Endothelium
Endothelium, Vascular - physiopathology
Enzymes
Health risks
Heart attack
Homocysteine
Homocysteine - blood
Humans
Hyperhomocysteinemia - complications
Ischemia
Nitric oxide
Nitric Oxide - pharmacokinetics
Oxidative Stress
Review Article
Risk Factors
Vascular diseases
Vasodilation
Vasodilation - drug effects
Vasodilator agents
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:This review discussed and in particular emphasis the potential cellular pathways and the biological processes involved that lead to homocysteine-induced endothelial dysfunction, in particular in the impaired endothelial dependent dilatation aspect. Hyperhomocysteinemia is an independent cardiovascular risk factor that has been associated with atherosclerotic vascular diseases and ischemic heart attacks. The potential mechanisms by which elevated plasma homocysteine level leads to reduction in nitric oxide bioavailability include the disruptive uncoupling of nitric oxide synthase activity and quenching of nitric oxide by oxidative stress, the enzymatic inhibition by asymmetric dimethylarginine, endoplasmic reticulum stress with eventual endothelial cell apoptosis, and chronic inflammation/prothrombotic conditions. Homocysteine-induced endothelial dysfunction presumably affecting the bioavailability of the potent vasodilator ‘nitric oxide’, and such dysfunction can easily be monitor by flow-mediated dilation method using ultrasound. Understanding the mechanisms by which plasma homocysteine alter endothelial nitric oxide production is therefore essential in the comprehension of homocysteine-induced impairment of endothelial dependent dilatation, and its association of cardiovascular risk and its pathophysiology.
ISSN:0250-6807
1421-9697
DOI:10.1159/000437098