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Heme Oxygenase-1: A Novel Therapeutic Target in Oxidative Tissue Injuries

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Oxidative stresses such as oxidant stimuli, inflammation, exposure to xenobiotics, or ionizing irradiation provoke cellular protective responses, principally involving transcriptional activation of genes encoding proteins which participate in the defense against oxidative tissue injuries. Excess of free heme, which is released from hemeproteins under such conditions, may constitute a major threat because it can catalyze the formation of reactive oxygen species (ROS). Exposure of mammalian cells to oxidative stimuli induces heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme degradation, as well as a 33-kDa heat shock protein. In various model systems, HO-1 induction confers protection on tissues from further injuries, while the abrogation of its induction accelerates cellular injuries. In this article, we review recent advances in the regulatory mechanism of ho-1 gene expression and the role of HO-1 in various models of experimental oxidative tissue injuries, and its potential therapeutic implications.

Keywords: acute hepatic injury; acute renal injury; heme; heme oxygenase-1; oxidative stress; sepsis; tin chloride; volatile anesthetics

Document Type: Review Article


Affiliations: Department of Anesthesiology and Resuscitology, Okayama University Medical School, 2-5-1 Shikata-cho Okayama, 700-8558, Japan

Publication date: 2004-06-01

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  • Current Medicinal Chemistry covers all the latest and outstanding developments in medicinal chemistry and rational drug design. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of the current topics in medicinal chemistry. Current Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments.
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