ArticleNature communications2024
The lncRNA SNHG26 drives the inflammatory-to-proliferative state transition of keratinocyte progenitor cells during wound healing.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Time to Heal: MicroRNA Temporal Dysregulation in Diabetic Foot Ulcers.International journal of molecular sciences · 2026Review
- Polysaccharide-engineered mitochondria reprogram macrophages to resolve diabetic wound inflammation and promote repair.Bioactive materials · 2026Article
- Trimodal, uncertainty-guided whole-slide framework for genome-scale spatial expression and image-only virtual perturbation in cancer cohorts.Genome medicine · 2026Article
- Evaluating the Antioxidant, Cytoprotective and Wound-Healing-Associated Effects ofInternational journal of molecular sciences · 2026Article
- Identification of Skin Multicellular Reprogramming Factors as Potential Treatment for Nonhealing Diabetic Foot Ulcers.Advances in wound care · 2026Article
- Human lncRNA, hLinfRNA7 (IDO1-AS) Regulates Cytokine Expression, Tryptophan Catabolism, and Inflammatory Response in Macrophage.Molecular and cellular biology · 2026Article
- Single-cell mapping of diabetic foot ulcers: mechanistic axes and therapeutic targets.Frontiers in medicine · 2026Review
- MFGE8-primed fibroblasts reprogram the immunosuppressed microenvironment to promote diabetic wound healing.Frontiers in cell and developmental biology · 2026Article
- Cellular and Molecular Mechanisms of Wound Repair: From Biology to Therapeutic Innovation.Cells · 2025Review
- Non-Coding RNAs and Their Role in Maintaining Epidermal Homeostasis.Current issues in molecular biology · 2025Review
- Snord15b Maintains Stemness of Intestinal Stem Cells via Enhancement of Alternative Splicing of Btrc Short Isoform for Suppression of β-Catenin Ubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Ultra-short cyclic peptide CyZoological research · 2025Article
- Major Common Hallmarks and Potential Epigenetic Drivers of Wound Chronicity and Recurrence: Hypothesis and Reflections.International journal of molecular sciences · 2025Review
- Snhg18 regulates Yap subcellular localization to maintain bone homeostasis.Nature communications · 2025Article
- Association of Blood Heavy Metals with Diabetic Foot Ulcers in U.S. Adults with Diabetes: Insights from the 1999-2004 NHANES Data.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025Article
- Comprehensive wound healing using ETN@FeJournal of nanobiotechnology · 2025Article
- mCellular and molecular life sciences : CMLS · 2025Article
- HSPA2 influences the differentiation and production of immunomodulatory mediators in human immortalized epidermal keratinocyte lines.Cell death & disease · 2025Article
- LINC01711 modulates proliferation, migration, and extracellular matrix deposition of hypertrophic scar fibroblasts by targeting miR-34a-5p.Archives of dermatological research · 2025Article
- A dynamically phase-adaptive regulating hydrogel promotes ultrafast anti-fibrotic wound healing.Nature communications · 2025Article
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Authors and funding
18 authors.
Funding
Abstract
The cell transition from an inflammatory phase to a subsequent proliferative phase is crucial for wound healing, yet the driving mechanism remains unclear. By profiling lncRNA expression changes during human skin wound healing and screening lncRNA functions, we identify SNHG26 as a pivotal regulator in keratinocyte progenitors underpinning this phase transition. Snhg26-deficient mice exhibit impaired wound repair characterized by delayed re-epithelization accompanied by exacerbated inflammation. Single-cell transcriptome analysis combined with gain-of-function and loss-of-function of SNHG26 in vitro and ex vivo reveals its specific role in facilitating inflammatory-to-proliferative state transition of keratinocyte progenitors. A mechanistic study unravels that SNHG26 interacts with and relocates the transcription factor ILF2 from inflammatory genomic loci, such as JUN, IL6, IL8, and CCL20, to the genomic locus of LAMB3. Collectively, our findings suggest that lncRNAs play cardinal roles in expediting tissue repair and regeneration and may constitute an invaluable reservoir of therapeutic targets in reparative medicine.
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