期刊
FRONTIERS IN BIOSCIENCE-LANDMARK
卷 16, 期 -, 页码 2372-2388出版社
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/3860
关键词
Atherosclerosis; Inflammation; Innate Immunity; Adaptive Immunity; Heme Oxygenase-1; Heme; Carbon Monoxide; Biliverdin; Bilirubin; Immune Cells; Review
资金
- National Institutes of Health [HL59976, HL74966]
- American Heart Association Midwest Affiliate
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.
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