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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 represents a common pathological outcome in the progression of chronic kidney disease (CKD) to end-stage renal disease, with profound remodeling of the tissue microenvironment serving as a key driver. While injured renal tubular epithelial cells play a pivotal role in remodeling the tissue microenvironment, it remains unclear whether and how the extracellular matrix components secreted by these cells mediate tubular-interstitial crosstalk. In this study, we demonstrate that Fibrillin-1 (FBN1), ectopically secreted by injured tubular cells, is a critical mediator of tubular-fibroblast crosstalk in the fibrotic microenvironment. Furthermore, we explore an innovative therapeutic strategy targeting the FBN1-enriched fibrogenic niche.
Two classical renal fibrosis models, unilateral ischemia-reperfusion injury (UIRI) and unilateral ureteral obstruction (UUO), were employed. Spatial transcriptomics (ST) was utilized to decipher cell crosstalk patterns post-kidney injury. Decellularized kidney tissue scaffolds (dKTS) were used to mimic the renal pathological microenvironment in vitro. Rat fibroblast cells (NRK-49F) were stimulated with recombinant FBN1 protein. A combination of techniques, including RNA sequencing, inhibitor assays, co-immunoprecipitation (Co-IP), molecular dynamics simulation, and drug screening, was applied to investigate the mechanism by which FBN1 promotes fibroblast proliferation and activation and to establish a drug screening system targeting FBN1. A tubule-specific FBN1 knockout mouse model was generated. Multimodal assessment (RNA sequencing, histological staining, Western blotting, etc.) validated FBN1's regulatory role in fibroblast proliferation and activation.
Spatial transcriptomic analysis identified FBN1 as a crucial component of the fibrogenic niche. In vitro experiments confirmed that FBN1 induces fibroblast proliferation and activation. Mechanistic studies revealed that FBN1, by constituting the fibrogenic niche, activates the FBN1-EGFR-ERK1/2 signaling axis, thereby driving fibroblast proliferation and activation and mediating aberrant crosstalk between injured tubular cells and fibroblasts. Drug screening identified fucosterol, a natural compound derived from brown algae, as an effective antagonist of FBN1. Fucosterol disrupts the formation of the FBN1-enriched fibrogenic niche and subsequently inhibits aberrant ERK pathway activation and fibroblast proliferation.
This study systematically elucidates a novel mechanism whereby the extracellular matrix protein FBN1 acts as a critical bridge mediating aberrant crosstalk between injured tubular cells and fibroblasts, driving renal fibrosis via activation of the FBN1-EGFR-ERK1/2 signaling pathway. Furthermore, using fucosterol, we validated the therapeutic feasibility of targeting the FBN1-enriched fibrogenic niche. These findings provide important theoretical foundation and practical guidance for understanding the formation of the fibrogenic niche, intercellular crosstalk, and developing targeted therapies against the fibrogenic niche.
