The roles of cytochrome P450 metabolites of arachidonic acid in the regulation of vascular function
LAI Jin-Sheng1,2, CHEN Chen1,2,*
1Division of Cardiology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China;2Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiologic Disorders, Wuhan 430030, China
Abstract
Arachidonic acids (AA) widely exist in multiple organs and can be metabolized into small lipid molecules with strong biological functions through several pathways. Among them, epoxyeicosatrienoic acids (EETs) and 20-hydroxyeicosatetraenoic acid (20-HETE), which are produced by cytochrome P450 enzymes, have attracted a lot of attentions, especially in vascular homeostasis. The regulation of vascular function is the foundation of vascular homeostasis, which is mainly achieved by manipulating the vascular structure and biological function. In the past 30 years, the roles of EETs and 20-HETE in the regulation of vascular function have been widely explored. In this review, we discussed the effects of EETs and 20-HETE on angiogenesis and vascular inflammation, respectively. Generally, EETs can dilate blood vessels and inhibit vascular inflammation, while 20-HETE can induce vasoconstriction and vascular inflammation. Interestingly, both EETs and 20-HETE can promote angiogenesis. In addition, the roles of EETs and 20-HETE in several vascular diseases, such as hypertension and cardiac ischemia, were discussed. Finally, the therapeutic perspectives of EETs and 20-HETE for vascular diseases were also summarized.
Key words: arachidonic acid; cytochrome P450; EETs; 20-HETE; vascular function; vascular diseases
Received: 2021-02-20 Accepted: 2021-05-25
Corresponding author: 陈琛 E-mail: chenchen@tjh.tjmu.edu.cn
DOI: 10.13294/j.aps.2021.0059
Citing This Article:
LAI Jin-Sheng, CHEN Chen. The roles of cytochrome P450 metabolites of arachidonic acid in the regulation of vascular function. Acta Physiol Sin 2021; 73 (4): 631-645 (in Chinese with English abstract).