ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
The Diminution of R-Loops Generated by LncRNA DSP-AS1 Inhibits DSP Gene Transcription to Impede the Re-Epithelialization During Diabetic Wound Healing.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The role of R-loops-mediated epigenetic regulation in genome stability maintenance and disease pathogenesis: a systematic review.Epigenetics · 2026Pooled it
- Focal ischemia induces genome-wide accumulation of R-loops in the brain.Molecular therapy. Nucleic acids · 2026Article
- Multidimensional Regulatory Mechanisms and Targeted Therapeutic Strategies for Inhibited Keratinocyte Proliferation in Diabetic Wounds.Drug design, development and therapy · 2026Review
- The Diminution of R-Loops Generated by LncRNA DSP-AS1 Inhibits DSP Gene Transcription to Impede the Re-Epithelialization During Diabetic Wound Healing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mechanisms of microbial infection and wound healing in diabetic foot ulcer: pathogenicity in the inflammatory-proliferative phase, chronicity, and treatment strategies.Frontiers in endocrinology · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Re-epithelialization constitutes a critical stage in the intricate process of wound healing, yet its mechanisms in the context of diabetic wounds remain elusive. In this study, the role of the mesenchymal-epithelial transition (MET) vis-à-vis the epithelial-mesenchymal transition (EMT) of keratinocytes in diabetic wound re-epithelialization is investigated. The findings reveal an impediment in the MET process, rather than EMT, which significantly compromised re-epithelialization in diabetic wounds. Furthermore, Desmoplakin (DSP) gene expression, encoding a key desmosome protein, is down-regulated in diabetic rats. This down-regulation coincided with aberrant hypo-demethylation of the DSP promoter. The inhibition of DSP expression is linked to reduced occupancy of Ten-eleven translocation 3 (TET3) at the DSP promoter, consequently suppressing TET3-dependent DNA demethylation. Additionally, a novel lncRNA termed DSP-AS1is identified, which is antisense to DSP. Notably, DSP-AS1 expression is down-regulated in diabetic skin wounds, and it interacted with TET3, a DNA demethylase. Notably, DSP-AS1 is found to form R-loops, triple-stranded DNA:RNA hybrids, at the DSP promoter, facilitating TET3 localization to the DSP promoter. Collectively, the findings suggest that reduced R-loop formation by DSP-AS1 impairs DSP gene transcription by repressing TET3-mediated DNA demethylation. This disruption of the orchestrated re-epithelialization process contributes to refractory diabetic wound healing.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.