Heme oxygenase-1 is an essential cytoprotective component in oxidative tissue injury induced by hemorrhagic shock

Toru Takahashi, Hiroko Shimizu, Hiroshi Morimatsu, Kyoichiro Maeshima, Kazuyoshi Inoue, Reiko Akagi, Masaki Matsumi, Hiroshi Katayama, Kiyoshi Morita

研究成果査読

61 被引用数 (Scopus)

抄録

Hemorrhagic shock causes oxidative stress that leads to tissue injuries in various organs including the lung, liver, kidney and intestine. Excess amounts of free heme released from destabilized hemoproteins under oxidative conditions might constitute a major threat because it can catalyze the formation of reactive oxygen species. Cells counteract this by rapidly inducing the rate-limiting enzyme in heme breakdown, heme oxygenase-1 (HO-1), which is a low-molecular-weight stress protein. The enzymatic HO-1 reaction removes heme. As such, endogenous HO-1 induction by hemorrhagic shock protects tissues from further degeneration by oxidant stimuli. In addition, prior pharmacological induction of HO-1 ameliorates oxidative tissue injuries induced by hemorrhagic shock. In contrast, the deletion of HO-1 expression, or the chemical inhibition of increased HO activity ablated the beneficial effect of HO-1 induction, and exacerbates tissue damage. Thus, HO-1 constitutes an essential cytoprotective component in hemorrhagic shock-induced oxidative tissue injures. This article reviews recent advances in understanding of the essential role of HO-1 in experimental models of hemorrhagic shock-induced oxidative tissue injuries with emphasis on the role of its induction in tissue defense.

本文言語English
ページ(範囲)28-40
ページ数13
ジャーナルjournal of clinical biochemistry and nutrition
44
1
DOI
出版ステータスPublished - 1月 2009

ASJC Scopus subject areas

  • 医学(その他)
  • 栄養および糖尿病
  • 臨床生化学

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