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Therapeutic roles of carbon monoxide in intestinal ischemia‐reperfusion injury
Author(s) -
Katada Kazuhiro,
Takagi Tomohisa,
Uchiyama Kazuhiko,
Naito Yuji
Publication year - 2015
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12742
Subject(s) - medicine , heme oxygenase , reperfusion injury , endogeny , pathogenesis , immune system , heme , ischemia , immunology , inflammation , intestinal ischemia , intestinal mucosa , gastrointestinal tract , biology , biochemistry , enzyme
Abstract Intestinal ischemia‐reperfusion ( I ‐ R ) injury is a complex, multifactorial, pathophysiological process with high morbidity and mortality, leading to serious difficulty in treatment. The mechanisms involved in the pathogenesis of intestinal I ‐ R injury have been examined in detail and various therapeutic approaches for intestinal I ‐ R injury have been developed; however, existing circumstances have not yet led to a dramatic change of treatment. Carbon monoxide ( CO ), one of the by‐products of heme degradation by heme oxygenase ( HO ), is considered as a candidate for treatment of intestinal I ‐ R injury and indeed HO ‐1‐derived endogenous CO and exogenous CO play a pivotal role in protecting the gastrointestinal tract from intestinal I ‐ R injury. Interestingly, anti‐inflammatory effects of CO have been elucidated sufficiently in various cell types including endothelial cells, circulating leukocytes, macrophages, lymphocytes, epithelial cells, fibroblast, organ‐specific cells, and immune‐presenting cells. In this review, we herein focus on the therapeutic roles of CO in intestinal I ‐ R injury and the cell‐specific anti‐inflammatory effects of CO , clearly demonstrating future therapeutic strategies of CO for treating intestine I ‐ R injury.