ArticleJournal of advanced research2026
OTUD1 delays wound healing by regulating endothelial function and angiogenesis in diabetic mice.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Ubiquitination-driven fibroblast dysfunction: a multi-omics blueprint for precision diagnosis and therapy in diabetic foot ulcer.Scientific reports · 2026Article
- β‑Ecdysone-Loaded Gelatin Methacryloyl Hydrogel Accelerates Diabetic Wound Healing by Improving Angiogenesis.ACS omega · 2026Article
- A platelet-rich plasma-loaded chitosan-based hydrogel for promoting type 2 diabetes wound healing.iScience · 2026Article
- Ubiquitination modifications as central regulators of metabolic dysfunction in type 2 diabetes mellitus.Frontiers in endocrinology · 2026Review
- A miRNA cocktail orchestrates coordinated cellular responses to promote diabetic wound healing.Burns & trauma · 2025Article
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Authors and funding
13 authors.
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Abstract
introductionDiabetic non-healing wounds represent a major complication of diabetes, primarily due to impaired angiogenesis. Ovarian tumor deubiquitinase 1 (OTUD1), a deubiquitinase, has been implicated in vascular pathophysiology; however, its role in endothelial dysfunction and angiogenesis during diabetic wound healing is still poorly understood.
objectivesThis study explores whether OTUD1 influences angiogenesis and its underlying mechanisms.
methodsWe developed OTUD1 knockout mice and induced type 1 and type 2 diabetes mellitus (T1DM and T2DM) by administering streptozotocin (STZ) alone or in combination with a high-fat diet (HFD), respectively. Human umbilical vein endothelial cells (HUVECs) incubated with high glucose and palmitic acid (HG + PA) were utilized to imitate hyperglycemia-induced endothelial dysfunction in vitro. Mass spectrometry combined with immunoprecipitation analysis was used to analyze the interacting proteins of OTUD1. Moreover, we developed endothelial-specific OTUD1 knockdown db/db mice using an adeno-associated virus serotype 2/BI30 (AAV2/BI30) vector.
resultsIncreased OTUD1 expressions were observed both in diabetic wound tissues and in HUVECs treated with HG + PA. OTUD1 deficiency promoted angiogenesis and fibrosis in wound tissues of T1DM and T2DM mice and alleviated HG + PA-induced endothelial migration inhibition, tube formation impairment, and oxidative stress in HUVECs. Mechanistically, OTUD1 directly interacted with β-catenin, reducing its K63-linked ubiquitination at residues K496, K508, and K625 via its catalytic site C320. This modification facilitated β-catenin phosphorylation, restricted its nuclear translocation, and downregulated the expression of angiogenesis-related factors. Finally, pharmacological inhibition of β-catenin reversed the improvement of delayed wound healing induced by OTUD1 knockdown in db/db mice.
conclusionThese findings elucidate the OTUD1-β-catenin pathway's role in endothelial dysfunction-associated angiogenesis and suggest OTUD1 as a promising therapeutic target for diabetic non-healing wounds.
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