The resolution of inflammation through omega-3 fatty acids in atherosclerosis, intimal hyperplasia, and vascular calcification

被引：69

作者：

Carracedo, Miguel ^{[1
]}

Artiach, Gonzalo ^{[1
]}

Arnardottir, Hildur ^{[1
]}

Back, Magnus ^{[1
,2
]}

机构：

[1] Karolinska Inst, Translat Cardiol, Dept Med, Neo, Stockholm, Sweden

[2] Karolinska Univ Hosp, Theme Heart & Vessels, Div Coronary & Valvular Heart Dis, M85, S-14186 Stockholm, Sweden

来源：

SEMINARS IN IMMUNOPATHOLOGY | 2019年 / 41卷 / 06期

关键词：

Inflammation; Lipoxygenase; Resolvins; Vascular injury; PRORESOLVING LIPID MEDIATORS; SMOOTH-MUSCLE-CELLS; POLYUNSATURATED FATTY-ACIDS; ASPIRIN-TRIGGERED LIPOXIN; CORONARY-ARTERY-DISEASE; NEOINTIMAL HYPERPLASIA; RESOLVIN D1; LEUKOTRIENE; PROGRESSION; RECEPTOR;

D O I：

10.1007/s00281-019-00767-y

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Omega-3 fatty acids serve as the substrate for the formation of a group of lipid mediators that mediate the resolution of inflammation. The cardiovascular inflammatory response in atherosclerosis and vascular injury is characterized by a failure in the resolution of inflammation, resulting in a chronic inflammatory response. The proresolving lipid mediator resolvin E1 (RvE1) is formed by enzymatic conversion of the omega-3 fatty acid eicosapentaenoic acid (EPA), and signals resolution of inflammation through its receptor ChemR23. Importantly, the resolution of cardiovascular inflammation is an active, multifactorial process that involves modulation of the immune response, direct actions on the vascular wall, as well as close interactions between macrophages and vascular smooth muscle cells. Promoting anti-atherogenic signalling through the stimulation of endogenous resolution of inflammation pathways may provide a novel therapeutic strategy in cardiovascular prevention.

引用

页码：757 / 766

页数：10

共 77 条

[1] N-3 fatty acids inhibit vascular calcification via the p38-mitogen-activated protein kinase and peroxisome proliferator-activated receptor-γ pathways [J].