ArticleOxidative medicine and cellular longevity2022
Exploration of the Protective Mechanism of Bax Removal against Ischemia Reperfusion Injury of Skin Flap through the p38 Mitogen-Activated Protein Kinase Pathway.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 5 citations in OpenAlex.
- Effects of extremely low-frequency sinusoidal electromagnetic field therapy on survival and vascularization in a rat random-pattern skin flap model.JPRAS open · 2026Article
- Targeting Programmed Cell Death in Flap Ischemia/Reperfusion Injury.Biomolecules · 2025Review
- Promotion of Random Flap Neovascularisation in Rats with Diabetes Using Botulinum Toxin Type A Through the HIF-1α/VEGF Pathway.Clinical, cosmetic and investigational dermatology · 2025Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
This research is aimed at exploring the influences of the Bax gene in the p38 mitogen-activated protein kinase (MAPK) pathway and its protective mechanism against ischemia-reperfusion injury (IRI) of skin flap. Forty male Sprague-Dawley (SD) rats were equally divided into the experimental group (Bax gene knockout rats) and control group. The dorsal flap model was prepared, and the survival rate of flap was observed after surgery. The rat flap tissue was cut and stained with hematoxylin-eosin (HE) and in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The distribution characteristics of p38MAPK and Bax were detected to evaluate the protective mechanism of Bax gene knockout on IRI of skin flap. After surgery, the survival rate of flaps in the experimental group (82.32%, 70.28%) was significantly higher than that in the control group (57.64%, 46.14%) (
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