Protective role of heme oxygenase-1 against inflammation in atherosclerosis

被引:68
作者
Durante, William [1 ]
机构
[1] Univ Missouri, Sch Med, Dept Med Pharmacol & Physiol, Columbia, MO 65211 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2011年 / 16卷
基金
美国国家卫生研究院;
关键词
Atherosclerosis; Inflammation; Innate Immunity; Adaptive Immunity; Heme Oxygenase-1; Heme; Carbon Monoxide; Biliverdin; Bilirubin; Immune Cells; Review; SMOOTH-MUSCLE-CELLS; CORONARY-ARTERY-DISEASE; ADHESION MOLECULE-1 EXPRESSION; INHALED CARBON-MONOXIDE; E-DEFICIENT MICE; GENE-TRANSFER; MAST-CELLS; ENDOTHELIAL-CELLS; HEART-DISEASE; MICROSATELLITE POLYMORPHISM;
D O I
10.2741/3860
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Heme oxygenase-1 (HO-1) catalyzes the first and rate-limiting step in the metabolism of free heme into equimolar amounts of ferrous iron, carbon monoxide (CO), and biliverdin. Biliverdin is subsequently converted to bilirubin by biliverdin reductase. HO-1 has recently been identified as a promising therapeutic target in the treatment of vascular inflammatory disease, including atherosclerosis. HO-1 represses inflammation by removing the pro-inflammatory molecule heme and by generating CO and the bile pigments, biliverdin and bilirubin. These HO-1 reaction products are capable of blocking innate and adaptive immune responses by modifying the activation, differentiation, maturation, and/or polarization of numerous immune cells, including endothelial cells, monocytes/macrophages, dendritic cells, T lymphocytes, mast cells, and platelets. These cellular actions by CO and bile pigments result in diminished leukocyte recruitment and infiltration, and pro-inflammatory mediator production within atherosclerotic lesions. This review highlights the mechanisms by which HO-1 suppresses vascular inflammation in atherosclerosis, and explores possible therapeutic modalities by which HO-1 and its reaction products can be employed to ameliorate vascular inflammatory disease.
引用
收藏
页码:2372 / 2388
页数:17
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