ArticleJournal of biomedical science2025
miR-200c inhibition and catalase accelerate diabetic wound healing.
Article in Journal of biomedical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026Review
- Multifunctional Hydrogels for Diabetic Wound Healing: Design Strategies and Microenvironmental Remodeling Mechanisms.Gels (Basel, Switzerland) · 2026Review
- Waste-to-Treasure: Nanozyme-Integrated Photocatalytic Microneedles Reconfigure Diabetic Burn Wounds via Endogenous Glucose-to-HResearch (Washington, D.C.) · 2026Article
- A catalase nanocapsule inhibits VSMCs proliferation and migration through PTEN/NLRP3 pathway.Frontiers in pharmacology · 2026Article
- Metabolic reprogramming in diabetic complications: mechanisms, pathologies, and molecular evidence from multi-organ studies.Frontiers in immunology · 2026Review
- Hypoxia preconditioned MSC exosomes attenuate high-altitude cerebral edema via the miR-125a-5p/RTEF-1 axis to protect vascular endothelial cells.Bioactive materials · 2025Article
- Major Common Hallmarks and Potential Epigenetic Drivers of Wound Chronicity and Recurrence: Hypothesis and Reflections.International journal of molecular sciences · 2025Review
- Customized Hydrogel System for the Spatiotemporal Sequential Treatment of Periodontitis Propelled by ZEB1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- New insights into microRNA in dermatological diseases.Frontiers in medicine · 2025Review
- Exosomal non-coding RNAs: a new avenue for treating diabetic foot ulcers.Frontiers in molecular biosciences · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
backgroundReactive oxygen species (ROS) are increased in diabetic conditions and play a causal role in diabetic foot ulcers (DFU). We previously showed that ROS up-regulate miR-200c expression, that in turns causes apoptosis, senescence, ROS upregulation and nitric oxide decrease, leading to endothelial disfunction.
methodsThe aim of this study is to dissect miR-200c role in DFU and to explore the potential role of anti-miR-200c and antioxidant catalase (CAT) in promoting wound healing (WH). miR-200c inhibition and CAT treatment were performed either in immortalized keratinocytes (HaCaT) or in primary fibroblasts (FBs) and keratinocytes (KCs) deriving from diabetic patients (pts) undergoing amputations. Primary cells deriving from pts undergoing saphenectomies were used as controls. The miR-200c blockade was performed either via lentiviral particles bearing an anti-miR-200c sequence or locked nucleic acid (LNA) anti-miR-200c oligos. Equine CAT was administered on cell medium. The WH assay was performed in vivo on diabetic (db/db) mice by a topical treatment with CAT and LNA anti-miR-200c on wounds dissolved in a Pluronic gel mixture, administered every three days.
resultsWe found that miR-200c levels were increased by different stimuli known to induce ROS, such as ultraviolet radiation (UV), hydrogen peroxide (H
conclusionsAnti-miR-200c and CAT could be considered a novel treatment for DFU and, possibly, for other types of non-diabetic skin ulcers.
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