Mechanisms of Cell Protection by Heme Oxygenase-1

被引：1032

作者：

Gozzelino, Raffaella ^{[1
]}

Jeney, Viktoria ^{[1
]}

Soares, Miguel P. ^{[1
]}

机构：

[1] Inst Gulbenkian Ciencias, Oeiras, Portugal

来源：

ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY | 2010年 / 50卷

关键词：

free radicals; cell death; inflammation; immune-mediated inflammatory diseases; NF-KAPPA-B; HEMOGLOBIN SCAVENGER RECEPTOR; SITE-SPECIFIC PHOSPHORYLATION; ENDOPLASMIC-RETICULUM-STRESS; ISCHEMIA-REPERFUSION INJURY; TRANSCRIPTION FACTOR BACH1; CARBON-MONOXIDE PROTECTS; ALPHA-INDUCED APOPTOSIS; SMOOTH-MUSCLE-CELLS; TOLL-LIKE RECEPTOR;

D O I：

10.1146/annurev.pharmtox.010909.105600

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

Heme oxygenases (140) catabolize free heme, that is, iron (Fe) protoporphyrin (IX), into equimolar amounts of Fe2+, 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.

引用

页码：323 / 354

页数：32

共 234 条

[41]

CARRELL RW, 1980, TEX REP BIOL MED, V40, P431

[42]

The E3 ubiquitin ligase itch couples JNK activation to TNFα-induced cell death by inducing c-FLIPL turnover [J].