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血红素加氧酶-1 的细胞保护机制。

Mechanisms of cell protection by heme oxygenase-1.

机构信息

Instituto Gulbenkian de Ciência, Oeiras, Portugal.

出版信息

Annu Rev Pharmacol Toxicol. 2010;50:323-54. doi: 10.1146/annurev.pharmtox.010909.105600.

DOI:10.1146/annurev.pharmtox.010909.105600
PMID:20055707
Abstract

Heme oxygenases (HO) catabolize free heme, that is, iron (Fe) protoporphyrin (IX), into equimolar amounts of Fe(2+), carbon monoxide (CO), and biliverdin. The stress-responsive HO-1 isoenzyme affords protection against programmed cell death. The mechanism underlying this cytoprotective effect relies on the ability of HO-1 to catabolize free heme and prevent it from sensitizing cells to undergo programmed cell death. This cytoprotective effect inhibits the pathogenesis of a variety of immune-mediated inflammatory diseases.

摘要

血红素加氧酶(HO)可分解游离血红素,即铁(Fe)原卟啉(IX),生成等摩尔量的 Fe(2+)、一氧化碳(CO)和胆绿素。应激反应性 HO-1 同工酶可提供对细胞程序性死亡的保护。这种细胞保护作用的机制依赖于 HO-1 分解游离血红素的能力,并防止其使细胞对细胞程序性死亡敏感。这种细胞保护作用抑制了多种免疫介导的炎症性疾病的发病机制。

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