Heme oxygenase-1: from biology to therapeutic potential

被引：201

作者：

Soares, Miguel P. ^{[1
]}

Bach, Fritz H. ^{[2
]}

机构：

[1] Inst Gulbenkian Ciencias, P-2780156 Oeiras, Portugal

[2] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA

来源：

TRENDS IN MOLECULAR MEDICINE | 2009年 / 15卷 / 02期

基金：

美国国家卫生研究院;

关键词：

CARBON-MONOXIDE PROTECTS; ALPHA-INDUCED APOPTOSIS; OXIDATIVE STRESS; BILIVERDIN REDUCTASE; MICROSATELLITE POLYMORPHISM; ENDOTHELIAL-CELLS; SERUM BILIRUBIN; GENE PROMOTER; ANTIOXIDANT; FERRITIN;

D O I：

10.1016/j.molmed.2008.12.004

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) is a stress-responsive enzyme that catabolizes free heme into carbon monoxide, iron (which induces the expression of heavy-chain ferritin, an iron-sequestering protein) and biliverdin (which is converted to bilirubin by biliverdin reductase). Over the past few years it has become apparent that these 'arms' of the HO-1 system can act protectively in a variety of experimental models of disease; there is also evidence that HO-1 and bilirubin have protective actions in humans. Here, we present a model for the beneficial actions of the products of heme degradation, and we discuss the potential clinical applications of enhancing the HO-1 system.

引用

页码：50 / 58

页数：9

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