ArticleWorld journal of diabetes2025
N6-methyladenosine methyltransferase Wilms tumor 1-associated protein impedes diabetic wound healing through epigenetically activating DNA methyltransferase 1.
Article in World journal of diabetes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Therapeutic implications of epigenetic alterations in burns: a new frontier in burn medicine.Clinical science (London, England : 1979) · 2026Review
- Role of the DNA methyltransferases in diabetes mellitus and Its complications.Molecular biology reports · 2026Review
- Crosstalk between gut microbiota and RNA N6-methyladenosine modification in diabetic retinopathy.Frontiers in cell and developmental biology · 2026Review
- Epigenetics and diabetic wound healing: Wilms tumor 1-associated protein as a therapeutic target.World journal of diabetes · 2025Article
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8 authors.
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Abstract
backgroundDiabetic wound injury is a significant and common complication in individuals with diabetes. N6-methyladenosine (m6A)-related epigenetic regulation is widely involved in the pathogenesis of diabetes complications. However, the function of m6A methyltransferase Wilms tumor 1-associated protein (WTAP) in diabetic wound healing remains elusive.
aimTo investigate the potential epigenetic regulatory mechanism of WTAP during diabetic wound healing.
methodsHuman umbilical vein endothelial cells (HUVECs) were induced with high glucose (HG) to establish
resultsThe expression of several m6A methyltransferases, including METTL3, METTL14, METTL16, KIAA1429, WTAP, and RBM15, were measured. WTAP exhibited the most significant elevation in HG-induced HUVECs compared with the normal control. WTAP depletion notably restored cell viability and enhanced tube formation ability and migration of HUVECs suppressed by HG. The unclosed wound area of mice was smaller in WTAP knockdown-treated mice than in control mice at nine days post-wounding, along with enhanced re-epithelialization rate and collagen deposition. The m6A levels on DNMT1 mRNA in HUVECs were repressed by WTAP knockdown in HUVECs. The mRNA levels and expression of DNMT1 were inhibited by WTAP depletion in HUVECs. Overexpression of DNMT1 in HUVECs notably reversed the effects of WTAP depletion on HG-induced HUVECs.
conclusionWTAP expression is elevated in HG-induced HUVECs and epigenetically regulates the m6A modification of DNMT1 to impair diabetic wound healing.
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