ArticleACS omega2026
Timed Epithelial Overlay Preserves Defect Closure While Suppressing Fibrotic Remodeling in Wound Microtissues.
Article in ACS omega, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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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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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Re-epithelialization restores barrier function and provides epithelial-derived paracrine signals that modulate fibroblast activation, contraction, and fibrotic remodeling. However, whether epithelial coverage can limit scar-like remodeling without compromising essential fibroblast-driven closure remains unclear. Here, we developed a tension-bearing NIH-3T3-collagen wound microtissue model supported by elastic scaffolds. A 500 μm circular microdefect was introduced to quantify epithelial regulation of closure dynamics and fibrotic remodeling. An MDCK epithelial overlay produced a strong, density-dependent inhibition of contraction-driven defect closure and suppressed the localized proliferative response at the wound edge. In contrast, delaying epithelial addition to 48 h postwounding preserved rapid closure while attenuating global microtissue compaction. This effect was partially mimicked by exogenous prostaglandin E
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Registered trials
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