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首页> 外文期刊>Frontiers in bioscience: a journal and virtual library >Protective role of heme oxygenase-1 against inflammation in atherosclerosis.
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Protective role of heme oxygenase-1 against inflammation in atherosclerosis.

机译：血红素加氧酶-1在动脉粥样硬化中对炎症的保护作用。

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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.
机译：血红素加氧酶-1（HO-1）催化游离血红素代谢成等摩尔量的亚铁，一氧化碳（CO）和胆绿素的第一步和限速步骤。随后，Biliverdin还原酶将Biliverdin转化为胆红素。 HO-1最近已被确定为治疗包括动脉粥样硬化在内的血管炎性疾病的有希望的治疗靶标。 HO-1通过去除促炎分子血红素并产生CO和胆色素，胆绿素和胆红素来抑制炎症。这些HO-1反应产物能够通过修饰众多免疫细胞（包括内皮细胞，单核细胞/巨噬细胞，树突状细胞，T淋巴细胞，肥大细胞）的激活，分化，成熟和/或极化来阻断先天性和适应性免疫反应。和血小板。 CO和胆汁色素的这些细胞作用导致动脉粥样硬化病变内白细胞募集和浸入的减少以及促炎性介质的产生。这篇综述着重介绍了HO-1抑制动脉粥样硬化中血管炎症的机制，并探讨了HO-1及其反应产物可用于缓解血管炎性疾病的可能的治疗方式。

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