Description
Title: Hypoxia-Induced Endothelial Dysfunction: The Effect of Low Oxygen on NO Bioavailability
Abstract: In the entire world, cardiovascular diseases (CVDs) are the main cause of death. Endothelial dysfunction, which is characterized by the restricted bioavailability of nitric oxide, characterizes the early stages of CVDs (NO). Therefore, the pathogenesis of CVD is affected by any factors that hinder the synthesis or metabolism of NO in endothelial cells. It is well known that hypoxia both initiates and accompanies cardiovascular disease, and that decreased tissue oxygen levels can affect the bioavailability of NO in endothelial cells. Tetrahydrobiopterin (BH4) serves as a crucial cofactor for the production of NO by endothelial nitric oxide synthase (eNOS) in endothelial cells from L-Arg. Here, we go over how hypoxia affects NO bioavailability, including how eNOS expression and activity are regulated. The fact that hypoxia causes the cofactor BH4 to be depleted and the substrate L-Arg to be deficient is particularly significant because this leads to eNOS uncoupling, a condition in which the enzyme produces superoxide instead of NO. Endothelial dysfunction and atherogenesis are primarily caused by eNOS uncoupling and the oxidative stress that results from it. Additionally, hypoxia causes impairment in mitochondrial respiration and endothelial cell activation, which together with the hypoxic response cause oxidative stress and inflammation, which in turn lead to the development of endothelial dysfunction.
Keywords: nitric oxide; eNOS; eNOS uncoupling; tetrahydrobiopterin; ADMA; hypoxia; cardiovas cular diseases
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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