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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.
Acute kidney injury (AKI) is a clinical syndrome involving a rapid decline in renal function. Tubular epithelial cells play a central role in AKI, and their regenerative capacity is crucial for functional recovery. However, the specific populations and states of proximal tubule (PT) cells that drive repair, along with their molecular regulation, remain poorly understood. In this study, we establish high-resolution spatiotemporal molecular landscapes of AKI by integrating large-scale spatial transcriptomic profiling (Stereo-seq) with single-nucleus RNA sequencing across multiple stages of disease progression.
The ischemic rat models of AKI were established by clamping bilateral renal arteries with non-traumatic vascular clip for 45 minutes. Then enhanced-resolution spatial transcriptomics (Stereo-seq) with snRNA-seq was conducted to profile kidney transcriptomes during AKI. Gene set enrichment analysis (GSEA) was used to identify signaling pathways and biological processes.
Our results demonstrated three high CytoTRACE-score clusters—proliferative PT, injured PT, and transitioning PT—is essential for elucidating the mechanisms underlying kidney regeneration during AKI. Gene set enrichment analysis (GSEA) reveals significant enrichment of the p38 MAPK signaling pathway and cellular response to hypoxia in the early stage, whereas Wnt signaling and kidney development-related functions were enriched in the late stage from injury to regeneration in proximal tubules. Furthermore, proliferative PT cells initiated renal regeneration and exhibited gene expression signatures associated with mitosis and metabolic processes.
In conclusion, our work redefines the heterogeneity of PT subpopulations and systematically elucidates their dynamic changes and functional roles throughout the processes of renal injury and repair following ischemia-reperfusion. By integrating high-resolution spatial and single-cell transcriptomic profiling, we constructed a comprehensive atlas that captures the spatiotemporal evolution of cell states during AKI. Through this approach, we identified a unique IRI-induced PT subtype localized specifically in the corticomedullary junction region, which exhibits elevated stemness properties and serves as a primary source for regenerating damaged tubular epithelium. Our study establishes an integrated, high-resolution map of AKI-induced alterations in the rat kidney, revealing previously unrecognized cellular transitions and niche-specific interactions.
