Heme oxygenase‑1 improves the survival of ischemic skin flaps (Review)
Zheng Y., Li Z., Yin M., Gong X.
Animal Study, published in Mol Med Rep (2021) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Mol Med Rep (2021)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 33537805
- PMCID
- PMC7893698
- DOI
- 10.3892/mmr.2021.11874
- Citations
- 7
Abstract (original English)
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.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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