ArticleEuropean journal of medical research2025
Continuous pressure exacerbates ischemia-reperfusion injury in minipigs through the AKT/eNOS signaling pathway.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Predictors of Pressure Injury Development and Clinical Course in ICU Patients: A Retrospective Cohort Study.Healthcare (Basel, Switzerland) · 2026Article
- ROS-responsive drug delivery systems for chronic wound healing: advances, challenges, and translational perspectives.Military Medical Research · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundPressure ulcers are localized injuries to the skin and subcutaneous tissue, often forming over bony prominences due to prolonged pressure or shear forces. These ulcers pose a significant health challenge, affecting nearly 3 million adults and creating a substantial healthcare burden.
objectivesThis study aimed to explore the pathological, inflammatory, fibrotic, and oxidative responses in skin subjected to ischemia-reperfusion injury (IRI) under different pressure conditions using a minipig model. MATERIALS AND
methodsMale minipigs (5-6 months old, 25-30 kg) were used to simulate IRI through varying pressure durations and intensities. Pathological assessments included collagen fiber disruption and damage to hair follicles and sebaceous glands. Inflammatory and oxidative responses were measured by analyzing microvessel density, glutathione peroxidase, superoxide dismutase, Vascular endothelial growth factor (VEGF), VEGF receptor 2, Hypoxia-inducible factor-1α(HIF-1α), Interleukin-1β(IL-1β), IL-6, Matrix Metalloproteinase-9 (MMP-9), MMP-1, cleaved caspase-3, phosphorylation RAC-alpha serine/threonine-protein kinase/Protein kinase B (p-AKT), and phosphorylation Endothelial Nitric Oxide Synthase (p-eNOS) levels.
resultsIncreasing pressure duration and intensity resulted in significant collagen fiber disruption and damage to hair follicles and sebaceous glands. There was a decline in microvessel density and levels of glutathione peroxidase, superoxide dismutase, VEGF, and VEGF receptor 2. Conversely, HIF-1α, IL-1β, IL-6, MMP-9, MMP-1, cleaved caspase-3, p-AKT, and p-eNOS levels increased.
conclusionExternal mechanical forces exacerbate ischemia-reperfusion injury in pressure ulcers by intensifying oxidative stress, inflammation, and fibrosis, mainly through the activation of the AKT/eNOS pathway.
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Registered trials
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