ArticleClinical science (London, England : 1979)2025
YTHDF2 regulates ACSL4-dependent ferroptosis of keratinocytes in diabetic wound healing.
Article in Clinical science (London, England : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Keratinocytes with DNA Aberration Induced by UVB Become Susceptible to Ferroptosis.Antioxidants (Basel, Switzerland) · 2026Article
- Chuangling Ye mitigates diabetic foot ulcer through suppressing keratinocyte ferroptosis via inhibiting ACSS2/ACSL4 axis.Chinese medicine · 2026Article
- Astragaloside IV in type 2 diabetic vascular complications: from traditional mechanisms to an emerging epitranscriptomic (m6A) perspective.American journal of translational research · 2026Review
- Integrated Bulk and Single-Cell Transcriptomics Reveals Cell-Type-Specific Fatty Acid Metabolic Dysregulation and Candidate Biomarkers in Diabetic Foot Ulcers.Clinical, cosmetic and investigational dermatology · 2026Article
- Autophagy-Ferroptosis Interplay Network: Redefining Therapeutic Paradigms for Diabetic Wound Healing.Journal of inflammation research · 2026Review
- From Dilemma to Breakthrough: Prospects for Clinical Application of Exosome-Hydrogel Systems in Diabetic Wound Repair.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnologyReview
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Authors and funding
11 authors.
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Abstract
Delayed diabetic wound healing is a global health issue with unclear pathogenesis. Ferroptosis, a form of cell death involving iron and lipid peroxidation, may contribute to delayed diabetic wound. This study investigates the role of ferroptosis in diabetic wound keratinocytes. We measured lipid peroxidation products (MDA, 4-HNE), ACSL4, and GPX4 protein levels in diabetic keratinocytes and assessed mitochondrial morphology. Ferrostatin-1 (Fer-1) was used to inhibit ferroptosis in diabetic rat wounds, and its effects on healing and expression levels were evaluated. Pull-down assays, silver staining, and mass spectrometry were employed to study ACSL4 mRNA regulation. A YTHDF2 knockdown adenovirus was used to manipulate YTHDF2 expression in rat wounds. Ferroptosis was detected in diabetic keratinocytes, hindering wound healing, a process reversible with Fer-1. High glucose induced ACSL4 expression, driving keratinocyte ferroptosis and delayed healing. YTHDF2 interacts with N6-methyladenosine-modified ACSL4 mRNA, affecting its stability and expression. YTHDF2 knockdown increased ACSL4, promoting ferroptosis and impairing healing. Our findings illustrate the significant involvement of ferroptosis in the dysfunction of diabetic keratinocytes, suggesting that targeting ferroptosis may offer a viable therapeutic approach for improving diabetic wound healing.
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