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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Renal fibrosis is the final common pathway of chronic kidney disease progression and a major driver of end-stage renal disease, yet no effective anti-fibrotic therapies exist. Fibroblast activation and extracellular matrix (ECM) deposition are central to this process, but the molecular regulators remain incompletely defined. We aimed to identify novel drivers of fibroblast activation using single-cell RNA sequencing (scRNA-seq) and to validate their functional relevance in renal fibrosis.
We reanalyzed a murine renal scRNA-seq dataset using pseudotime trajectory analysis to identify regulators of fibroblast activation. Among the top candidates, Capg emerged as a strong regulator correlating with ECM gene expression. CAPG expression was assessed in human biopsies and in murine models of folic acid nephropathy, unilateral ureteral obstruction (UUO), and ischemia-reperfusion injury (IRI). Functional relevance was tested in Capg–/– and fibroblast-specific Capgknockout mice. Mechanistic insights were obtained using scRNA-seq of Capg–/– kidneys and CUT&Tag sequencing in CAPG-overexpressing fibroblasts, complemented by immunoprecipitation, chromatin immunoprecipitation, and reporter assays. CAPG’s role beyond the kidney was evaluated in a carbon tetrachloride–induced liver fibrosis model.
Single-cell RNA-seq of the IRI-based mouse renal fibrosis dataset GSE180420 identified CAPG as highly expressed in activated fibroblasts. Differential expression analysis showed strong correlation between CAPG and profibrotic signatures. Global CAPG knockout reduced fibrosis severity, judged by Masson’s trichrome, Sirius Red, and fibrotic markers. scRNA-seq confirmed CAPG predominantly expression during fibrosis; its loss inhibited myofibroblast differentiation and ECM synthesis (Figure 1 a-e). CUT&Tag-seq in CAPG-overexpressing fibroblasts suggested CAPG regulates the TGF-β pathway and co-occupies Smad binding regions (Figure 1 f-i). Fibroblast-specific deletion of CAPG attenuated fibrosis and preserved renal function (Figure 2). Co-IP and ChIP-qPCR revealed CAPG interaction with Smad4 and CBP to drive profibrotic transcription, and luciferase assays verified CAPG enhancement of Smad4–CBP-mediated activation. CAPG knockout also attenuated CCl₄-induced liver fibrosis, assessed by Masson’s trichrome, Sirius Red, and fibrotic markers (Figure 3).
CAPG is a previously unrecognized regulator of fibroblast activation and ECM production that operates as a co-activator of TGF-β signaling via regulating Smad4-CBP interaction (Figure 4). Inhibition of CAPG protects against renal fibrosis and preserves renal function, while also attenuating hepatic fibrosis. CAPG emerges as a critical molecular driver of fibrosis across organs and a promising candidate for the development of targeted anti-fibrotic therapies.
