ArticleJournal of clinical biochemistry and nutrition2025
Ischemia/reperfusion-associated oxidative stress is an aggravating factor for pressure ulcers.
Article in Journal of clinical biochemistry and nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Inflammasome-derived biomarkers in wound healing: linking tissue repair, chronic inflammation, fibrosis, and precision therapeutics.Molecular biology reports · 2026Review
- Ginsenoside Rb1-engineered nanocomposite hydrogel promotes pressure injury repair through SIRT1-AMPK-mediated ferroptosis inhibition and angiogenesis activation.Journal of ginseng research · 2026Article
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2 authors.
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Abstract
Prolonged compression restricts blood flow, which can result in an insufficient supply of the oxygen and nutrients that are necessary for cells to live and thrive. A pressure ulcer (PU) is a pathological condition of prolonged ischemia and is associated with a loss of epidermis, which could expose the dermis and deeper tissues. It is necessary to remove the causative pressure and resume blood flow, but injurious damage to the ischemic area could occur with a delay after blood reflow, which could result in reperfusion injury. In the early stages of compression, muscle cells, which are highly dependent on aerobic respiration, are preferably damaged, and then the injury could spread to other dermal and epithelial cells. Infiltrated leukocytes release a variety of substances such as cytokines and reactive oxygen species (ROS) that act as anti-microorganisms, but these could also aggravate inflammation. The ROS are deeply involved in the pathogenesis of this condition, and, hence, antioxidant compounds and enzymes play a vital role in preventing the progression of PUs. We focus on oxidative stress in PUs, which is exacerbated by the actions of ischemia/reperfusion, and we discuss effective prevention and treatment from the perspectives of micronutrients and antioxidants.
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