ArticleCell death & disease2026
Beyond re-epithelialization: prolonged remodeling re-establishes epithelial homeostasis in oral mucosa.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- The airway epithelial-immune axis: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Wound healing restores tissue integrity through tightly coordinated cellular and molecular programs, yet the biological processes that persist after apparent closure remain largely unexplored. Using a standardized mouse hard palate injury model combined with histological, lineage-tracing, molecular, and epigenetic analyses, we show that rapid re-epithelialization is followed by months of cellular remodeling. Although wounds re-epithelialized within two weeks, temporal analyses revealed that the regenerated epithelium maintained leading-edge-like features for months. Structural reorganization, including increased cell density and epithelial thickness, persisted well beyond closure, accompanied by sustained proliferation and elevated apoptosis mediated by the p53-p21 pathway, thereby removing cells with DNA damage during tissue remodeling. Lineage tracing revealed marked alterations in Wnt-responsive epithelial stem cells, which were transiently lost from the repaired epithelium and gradually repopulated the tissue over approximately four months. Repair-activated keratinocytes showed sustained expression of keratin 6 and keratin 17 and delayed recovery of differentiation markers keratin 10 and filaggrin, indicating prolonged epithelial activation despite morphological closure. Coordinated alterations in histone marks H2AK119ub, H3K27ac, and H3K27me3, and persistent immune infiltration, indicate lasting molecular and microenvironmental remodeling that maintains the tissue in a memory-like state. Together, these findings indicate that oral wound healing is an extended, multi-phase process in which post-healing remodeling restores epithelial homeostasis and ensures proper resolution of the repair response.
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Registered trials
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