ArticleJournal of advanced research2026
JAM-C prevents ocular fibrosis by suppressing the TAZ/KLF6 pathway.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- An Inhibitory Aptamer Against PDGF-C Overcomes Anti-VEGF Refractoriness and Reduces Choroidal Neovascularization and Fibrosis.Investigative ophthalmology & visual science · 2026Article
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17 authors.
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No grant is acknowledged in the PubMed record.
Abstract
introductionOcular fibrosis is one of the leading causes of irreversible visual impairment or blindness. Currently, there is no effective drug available for such diseases. Therefore, understanding the underlying mechanisms is a prerequisite for finding better therapeutic strategies.
objectivesThis study aims to investigate the role of the junctional adhesion molecule C (JAM-C) in ocular fibrosis.
methodsThe protein levels of JAM-C were determined in the vitreous humor samples of patients with ocular fibrosis using ELISA. Jam-c genetic deletion mice and ocular fibrosis mouse models were generated to study the role of JAM-C in vivo. EMT, proliferation, migration, and gel contraction capacities in RPE cells were examined after JAM-C knockdown by siRNAs. RNA sequencing, co-IP, ChIP-qPCR, and luciferase reporter assay were performed to investigate the underlying mechanisms. Subretinal injection of adeno-associated virus, immunofluorescence, western blot were performed to evaluate the potential of JAM-C in preventing ocular fibrosis in different mouse models.
resultsMarkedly reduced JAM-C expression was found in patients with ocular fibrosis. Genetic deletion of Jam-c in mice exacerbated ocular fibrosis, and JAM-C knockdown triggered the EMT process in RPE cells. Mechanistically, we reveal that JAM-C inhibits ocular fibrosis by suppressing the nuclear localization and function of TAZ, which otherwise binds to KLF6 to promote its expression and activity to initiate the EMT cascade. Importantly, AAV-mediated JAM-C augmentation alleviated ocular fibrosis in different mouse models.
conclusionOur findings unveil a novel function of JAM-C in preventing ocular fibrosis by inhibiting the TAZ/KLF6 pathway, and suggest new therapeutic possibilities for the treatment of fibrotic diseases.
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