Heme oxygenase‑1 improves the survival of ischemic skin flaps (Review)

Heat shock protein 32 (Hsp32), also known as heme oxygenase‑1 (HO‑1), is an enzyme that exists in microsomes. HO‑1 can be induced by a variety of stimuli, including heavy metals, heat shock, inflammatory stimuli, heme and its derivatives, stress, hypoxia, and biological hormones. HO‑1 is the rate‑li...

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Published inMolecular medicine reports Vol. 23; no. 4
Main Authors Zheng, Yinhua, Li, Zhenlan, Yin, Min, Gong, Xu
Format Journal Article
LanguageEnglish
Published Greece Spandidos Publications 01.04.2021
Spandidos Publications UK Ltd
D.A. Spandidos
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Summary:Heat shock protein 32 (Hsp32), also known as heme oxygenase‑1 (HO‑1), is an enzyme that exists in microsomes. HO‑1 can be induced by a variety of stimuli, including heavy metals, heat shock, inflammatory stimuli, heme and its derivatives, stress, hypoxia, and biological hormones. HO‑1 is the rate‑limiting enzyme of heme catabolism, which splits heme into biliverdin, carbon monoxide (CO) and iron. The metabolites of HO‑1 have anti‑inflammatory and anti‑oxidant effects, and provide protection to the cardiovascular system and transplanted organs. This review summarizes the biological characteristics of HO‑1 and the functional significance of its products, and specifically elaborates on its protective effect on skin flaps. HO‑1 improves the survival rate of ischemic skin flaps through anti‑inflammatory, anti‑oxidant and vasodilatory effects of enzymatic reaction products. In particular, this review focuses on the role of carbon monoxide (CO), one of the primary metabolites of HO‑1, in flap survival and discusses the feasibility and existing challenges of HO‑1 in flap surgery.
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ISSN:1791-2997
1791-3004
DOI:10.3892/mmr.2021.11874