Recent developments on the vascular effects of 20-hydroxyeicosatetraenoic acid

被引:22
|
作者
Garcia, Victor [1 ]
Schwartzman, Michal L. [2 ]
机构
[1] Yale Univ, Dept Pharmacol, New Haven, CT USA
[2] New York Med Coll, Sch Med, Dept Pharmacol, 15 Dana Rd, Valhalla, NY 10595 USA
来源
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION | 2017年 / 26卷 / 02期
关键词
cytochrome P450; endothelial dysfunction; hypertension; stroke; vascular remodeling; CYTOCHROME P450-DERIVED EICOSANOIDS; ANGIOTENSIN-CONVERTING ENZYME; SALT-SENSITIVE HYPERTENSION; PHOSPHOLIPASE-D ACTIVATION; NITRIC-OXIDE PRODUCTION; ARACHIDONIC-ACID; BLOOD-PRESSURE; SMOOTH-MUSCLE; OMEGA-HYDROXYLASE; ENDOTHELIAL DYSFUNCTION;
D O I
10.1097/MNH.0000000000000302
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review 20-Hydroxyeicosatetraenoic acid (20-HETE) is a potent vasoactive eicosanoid and a key constituent of the microcirculation. Its effects on vascular function are multifaceted and include stimulation of smooth muscle, contractility, migration, and proliferation, as well as endothelial cell dysfunction and inflammation. Such effects have significant implications with regard to the control of vascular homeostasis and pathophysiology. The clinical relevance of 20-HETE is highlighted by recent studies linking 20-HETE and its biosynthetic enzymes to the development of hypertension, stroke, and myocardial infarction. Recent findings This article presents past and recent findings that focus on the role of 20-HETE in the regulation of the vasculature in health and disease and the implication of its actions on endothelial and vascular smooth muscle cells to the pathogenesis of hypertension and stroke. Summary To date clinical studies corroborated animal studies in that they place 20-HETE as a significant contributor to the pathogenesis of cardiovascular diseases. Consequently, uncovering 20-HETE effects in the vasculature along with understanding its mechanism of action provide a strong basis for the development of novel therapeutic strategies to prevent vascular/end organ damage in these diseases.
引用
收藏
页码:74 / 82
页数:9
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