ArticleMammalian genome : official journal of the International Mammalian Genome Society2025
Highly expressed TRIM32 promoted traumatic wound healing by mediating ubiquitination of PIAS1.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2025. 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.
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Who cites it
1 citing paper in PubMed.
- TRIM28 Promotes Keratinocyte Proliferation and Invasion by Activating NLRP3/SGT1 Axis-Mediated Macrophage Pro-Inflammatory Polarization in an In Vitro Macrophage-Keratinocyte Co-Culture Model.Immunity, inflammation and disease · 2026Article
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Authors and funding
2 authors.
Funding
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Abstract
Poor wound healing is a significant challenge that can result in lower limb amputation. Unfortunately, effective treatments are currently limited. Therefore, there is an urgent need to investigate new targets within the skin healing process to identify more effective treatment options. Differentially expressed genes (DEGs) were identified before and after wound healing based on the gene expression profiles GSE23006 and GSE21648 from the Gene Expression Omnibus database, and enrichment analysis of the DEGs was performed. And we found that a total of three differentially expressed genes (DEGs)-TFPI2, ELN, and TRIM32-were identified as key genes in the wound healing process. TRIM32 was selected for further study due to its high expression levels and significant variance in expression in an in vitro wound healing model. The overexpression of TRIM32 promoted skin fibroblast cells migration and epithelial-mesenchymal transition (EMT). Mechanistically, TRIM32 regulated the ubiquitination of PIAS1, leading to a reduction in PIAS1 protein expression. Additionally, TRIM32 has been shown to enhance wound healing by modulating PIAS1 expression. These findings highlight the beneficial role of TRIM32 in wound healing and tissue repair, suggesting that the TRIM32/PIAS1 axis may serve as a promising therapeutic target for enhancing wound healing.
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Registered trials
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