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Updated: Nov 18, 2025

Ischemic Tissue Injury in the Dorsal Skinfold Chamber of the Mouse: A Skin Flap Model to Investigate Acute Persistent Ischemia
Published on: November 17, 2014
Heme oxygenase‑1 improves the survival of ischemic skin flaps (Review)
Yinhua Zheng1, Zhenlan Li2, Min Yin3
1Department of Hand and Foot Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Abstract:
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.

