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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.
Progressive renal fibrosis represents a final common pathway of chronic kidney disease, often driven by maladaptive epithelial repair and senescence. We previously identified Protein Disulfide Isomerase Family A Member 3 (PDIA3) as a key regulator of extracellular matrix (ECM) turnover and fibroblast activation. Here, we explored the mechanistic connection between PDIA3, epithelial senescence, and fibrotic remodeling, and assessed the therapeutic potential of PDIA3 inhibition in vivo.
Unilateral ureteral obstruction (UUO) was induced in 12 mice to model renal fibrosis. Six animals received the PDIA3 inhibitor Loc14 (15 mg/kg, intraperitoneally in 10% DMSO) for 10 days post-surgery; six controls received vehicle only. Fibrosis was evaluated by histochemistry, immunofluorescence, and Western blotting. RT-qPCR assessed gene expression of profibrotic markers (Col1a1, FSP1). Single-slide quantitative proteomics was applied to identify pathways modulated by PDIA3 inhibition. Transcriptomic datasets from murine and human renal injury models were integrated to evaluate PDIA3 expression in senescent epithelial populations.
Loc14 treatment markedly attenuated tubular injury, collagen deposition, and glomerular fibrosis. Immunofluorescence confirmed reduced collagen-I accumulation, while Col1a1 and FSP1 were significantly downregulated. Proteomic profiling demonstrated suppression of TGFβ-1–dependent pathways and senescence-associated signaling cascades. Cross-species transcriptomic comparison revealed that PDIA3 is consistently overexpressed in senescent epithelial cells and augments TGFβ-mediated fibroblast activation. Pharmacologic PDIA3 inhibition disrupted this profibrotic crosstalk and promoted adaptive tissue repair.
PDIA3 acts as a central molecular mediator linking epithelial senescence to fibrogenic signaling and ECM remodeling. In vivo inhibition of PDIA3 with Loc14 effectively mitigates ongoing renal fibrosis by modulating TGFβ-1 and other fibrosis-associated pathways. These findings identify PDIA3 as a promising therapeutic target for the prevention and treatment of progressive kidney fibrosis.
