内皮型一氧化氮合酶脱偶联分子机制

Molecular Mechanisms of Endothelial Nitric Oxide Synthase Uncoupling

目的:内皮型一氧化氮合酶(eNOS)主要表达于血管内皮细胞中,是保护心血管系统的重要酶,当病理刺激因素作用于血管时,eNOS发生脱偶联,导致心血管疾病的发生发展。目前已明确的脱偶联机制包括四氢生物蝶呤(BH4)缺乏、L-精氨酸缺乏、锌指结构破坏、谷胱甘肽化、乙酰化、蛋白质-蛋白质相互作用及氮氧化合物4(NOX4)与内质网应激,本文就此内容进行综述。

Endothelial nitric oxide synthase （eNOS） is mainly expressed in vascular endothelial cells. It is an important enzyme to protect the cardiovascular system. When the pathological stimulant factors play a role in blood vessels, eNOS is deformed and leads to the development of cardiovascular disease. Are now clear to take off the coupling mechanisms include four hydrogen biopterin （BH4） lack, lack of L-arginine, zinc finger structure damage, glutathione, acetylation, protein-protein interactions, and nitrogen oxides 4 （NOX4） and endoplasmic reticulum stress, this paper summarized on the content.