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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.
The adhesion of podocytes—terminally differentiated epithelial cells—to the glomerular basement membrane is critical for kidney function. While adhesion disruption causes podocyte loss, the molecular mechanisms by which impaired focal adhesion drives progressive podocyte dysfunction and cell loss in glomerulosclerosis remain poorly understood.
We used doxycycline-inducible podocyte-specific Tln1 knockout (Tln1-cKO) mice, an established model of impaired focal adhesion, and performed single-cell RNA sequencing to identify early molecular changes. To investigate a key candidate gene, we generated podocyte-specific Nsf knockout (Nsf-cKO) mice and assessed them using cell spreading assays, morphological and molecular analyses, and live-cell imaging using the Retention Using Selective Hooks (RUSH) system.
Screening of Tln1-cKO podocytes revealed Nsf, which encodes N-ethylmaleimide-sensitive factor (NSF)—an AAA+ ATPase essential for vesicular trafficking by disassembling soluble NSF attachment protein receptor complexes—as one of the most significantly downregulated genes in injured podocytes. Podocyte-specific Nsf deletion resulted in massive proteinuria, podocyte loss, glomerulosclerosis, tubulointerstitial fibrosis, renal failure, and early mortality by 3 weeks. Nsf-cKO podocytes exhibited impaired cell spreading, with defective integrin α3 maturation and β1 proteasomal degradation. Our morphological analysis revealed an expanded endoplasmic reticulum (ER) and a disrupted Golgi structure. The RUSH assay demonstrated severely delayed ER-to-Golgi trafficking (90–120 min vs. 15 min). This transport defect and the resulting integrin phenotype were mimicked by pharmacological inhibition and rescued by NSF re-expression.
Our findings uncover a novel pathogenic pathway in which impaired podocyte adhesion downregulates NSF, resulting in severe disruption of ER-to-Golgi trafficking and compromised integrin maturation and stability. This mechanism creates a pathogenic cascade of progressive adhesion failure and glomerular disease. NSF-mediated protein trafficking emerges as a critical mechanism for maintaining podocyte homeostasis and represents a promising therapeutic target for proteinuric kidney diseases.
