ArticleInflammation2025
Targeting S100A12 to Improve Angiogenesis and Accelerate Diabetic Wound Healing.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Inflammation and wound healing: a comprehensive overview of mechanisms, therapeutic strategies, and translational perspectives.Biomarker research · 2026Review
- Article
- Identification and validation of novel inflammatory response-related diagnostic biomarkers in diabetic foot ulcers.Journal of diabetes investigation · 2026Article
- S100A12 drives inflammatory and metabolic reprogramming in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2026Review
- S100A12 as a key biomarker in a neutrophil-associated gene prediction model for sepsis diagnosis.Medicine · 2025Article
- A Boron-Based Topical Strategy for Enhancing Flap Survival: Mechanistic Insights Through Proteomic Analysis.Biomimetics (Basel, Switzerland) · 2025Article
- Serum S100A12 in the clinical diagnosis of sepsis-induced myocardial dysfunction: an integrated bioinformatics and clinical data analysis.Frontiers in cardiovascular medicine · 2025Article
- Targeting the AGEs-RAGE axis: pathogenic mechanisms and therapeutic interventions in diabetic wound healing.Frontiers in medicine · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
Long-term inflammation and impaired angiogenesis are thought to be the causes of delayed healing or nonhealing of diabetic wounds. S100A12 is an essential pro-inflammatory factor involved in inflammatory reactions and serves as a biomarker for various inflammatory diseases. However, whether high level of S100A12 exists in and affects the healing of diabetic wounds, as well as the underlying molecular mechanisms, remain unclear. In this study, we found that the serum concentration of S100A12 is significantly elevated in patients with type 2 diabetes. Exposure of stratified epidermal cells to high glucose environment led to increased expression and secretion of S100A12, resulting in impaired endothelial function by binding to the advanced glycation endproducts (RAGE) or Toll-like receptor 4 (TLR4) on endothelial cell. The transcription factor Krüpple-like Factor 5 (KLF5) is highly expressed in the epidermis under high glucose conditions, activating the transcriptional activity of the S100A12 and boost its expression. By establishing diabetic wounds model in alloxan-induced diabetic rabbit, we found that local inhibition of S100A12 significantly accelerated diabetic wound healing by promoting angiogenesis. Our results illustrated the novel endothelial-specific injury function of S100A12 in diabetic wounds and suggest that S100A12 is a potential target for the treatment of diabetic wounds.
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Registered trials
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