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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.
While significant progress has been made in understanding the mechanism of apoptosis in renal tubular epithelial cells (RTECs) and developing related targeted therapies for acute kidney injury (AKI), the development of effective and specific targeted therapies remains a challenge.
To explore potential targets for AKI, we exposed renal RTECs to a hypoxia/reoxygenation environment and conducted labeling-free proteomics. Then we demonstrated that signal recognition particle 14 (SRP14) induces apoptosis of renal tubular epithelial cells to exacerbate AKI involving interaction with ribosomal protein S7 (RPS7), and RPS7 is a potential target for Nafamostat mesylate to intervene AKI, as assessed by multiple techniques: measurement of tubule specific SRP14 knockout (SRP14-/-, Ggt-Cre) mice, Multiplex immunofluorescence staining of renal tissues, and flow cytometry, western blotting, ELISA, Immunoprecipitation, Protein purification, and Biolayer Interferometry.
The hypoxia/reoxygenation treatment significantly increased SRP14 in apoptotic RTECs. Notably, SRP14 was significantly elevated in the serum of patients with AKI, with an area under the receiver operating characteristic curve of 79.96%. Additionally, the SRP14 expression was significantly increased in the renal tubules of patients with acute tubular necrosis, as well as in four AKI mouse models following the procedures of ischemia-reperfusion injury (IRI), cecal ligation and puncture, and treatment with lipopolysaccharide and cisplatin. Moreover, SRP14 appears to play a crucial role in the apoptosis of RTECs, as evidenced by an IRI-induced AKI model in tubule-specific Srp14 knockout mice. Furthermore, SRP14 triggered apoptosis in renal tubules upon renal IRI via the RPS7-mediated tumor protein p53 (TP53)–MDM2 proto-oncogene (MDM2) pathway. Given the importance of RPS7 in SRP14-regulated apoptosis, we screened an apoptosis-specific library containing 356 US Food and Drug Administration–approved compounds to identify those that inhibit RPS7. We identified nafamostat mesilate as a potent RPS7 inhibitor that attenuated renal IRI by inhibiting RPS7-associated RTEC apoptosis.
These findings suggest that SRP14 triggers apoptosis in RTECs, thereby exacerbating AKI, by interacting with RPS7, which may be a potential therapeutic target for nafamostat mesylate to slow the progression of AKI.
