ArticleCommunications biology2024
SPRR1B+ keratinocytes prime oral mucosa for rapid wound healing via STAT3 activation.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
- OTUD6A-Mediated Deubiquitination of PRDX1 Protects Against Oral Ulcer by Restoring Mitochondrial Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Schwann cell derived extracellular vesicles are multifunctional nanotherapeutic mediators for diabetic oral mucosal wound healing.Discover nano · 2026Review
- Harnessing the Therapeutic Potential of Extracellular Vesicles for Oral Wound Healing.Bioengineering (Basel, Switzerland) · 2026Review
- Transcriptomic Differences Between Immortalized Oral and Skin Keratinocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Risk scoring model for lung adenocarcinoma based on PD-L1 related signature reveals prognostic predictability and correlation with tumor immune microenvironment genes was constructed.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Oral mucosal wounds exhibit accelerated healing with reduced scarring compared to cutaneous wounds, representing an optimal wound healing paradigm. However, the specific cellular subtypes orchestrating the efficient healing of mucosal tissues remain elusive. Through a comprehensive analysis integrating bulk-mRNA and single-cell sequencing data during the wound healing process in oral mucosa and skin, we have delineated a distinct set of genes markedly upregulated during tissue repair. This collection of wound healing-associated genesets was highly enriched in a specific keratinocyte subpopulation identified as STAT3-activated SPRR1B+ keratinocytes. Notably, despite the inherent rapidity of oral mucosal healing, the induction of SPRR1B+ keratinocytes is evident in both skin and mucosal wound healing processes in murine model. Intriguingly, these wound healing-promoting SPRR1B+ keratinocytes, which are induced via STAT3 activation, inherently abundant in unwounded normal mucosa but absent in normal skin. SPRR1B knockdown significantly inhibits mucosal keratinocyte migration, a critical attribute for effective wound healing. In summary, through analysis of human oral and skin wound healing processes at single-cell resolution, coupled with validation in murine model, suggests STAT3-activated SPRR1B+ keratinocytes are associated with the rapid mucosal repair process. This discovery underscores the potential application of SPRR1B+ keratinocytes in the therapeutic management of chronic or non-healing wounds.
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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.