ArticleInternational journal of molecular sciences2025
Hyperglycemia Induced in Sprague-Dawley Rats Modulates the Expression of CD36 and CD69 During Wound Healing.
Article in International journal of molecular sciences, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Advances and Challenges in the Comprehensive Management of Diabetic Foot: A Narrative Review from a General Practice Perspective.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Potential dietary geroprotectors and their impact on key mechanisms of aging.Biogerontology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Diabetic foot ulcers (DFUs) are a leading cause of morbidity worldwide along with the risk of other chronic health issues. Hyperglycemia has been shown to alter immune regulation at the wound site and potentially contributes to non-healing DFUs. However, the effects of hyperglycemia on the expression of mediators of inflammation and angiogenesis (CD36), immune regulation (TLR-7 and CD69), and inflammation/tissue repair (CD274) regarding wound healing are unknown. This study aims to investigate the effects of hyperglycemia on the gene and protein expression of CD36, CD69, CD274, and TLR-7 during wound healing using a rat model of induced diabetes. The expression of these mediators was examined using cutaneous tissues from rat models of diabetes with cutaneous wounds. Skin samples
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