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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 prevalent clinical syndrome marked by a sudden loss of renal function and acute tubular necrosis. However, the underlying mechanisms of AKI remain poorly understood, and effective therapies are still lacking. Here we report that Annexin A13 (ANXA13), the founder member of Annexins, is renal protective in AKI.
Kidney specimens, serum and urine of AKI patients were collected to detect the changes of ANXA13 during AKI. Then, ischemia-reperfusion injury (IRI) and cisplatin-induced AKI was established in ANXA13-overexpressing and renal tubule-specific ANXA13 knockout mice. Furthermore, the protective mechanisms of ANXA13 in AKI were investigated by RNA-seq, Co-IP and Chip assay.
Clinically, ANXA13 was lost in the kidney of AKI patients and mice with ischemic-reperfusion injury (IRI)- or cisplatin-induced AKI. This was associated with declined serum ANXA13 and elevated urinary ANXA13. Functionally, overexpressing ANXA13 conferred protection against but knockout of ANXA13 promoted IRI- and cisplatin-induced AKI. Mechanistically, we uncovered that ANXA13 could directly bind to TGF-β receptor type 1 intracellular domain and inhibited its phosphorylation, thereby inactivating Smad3 signaling and Smad3-mediated tubular cell death via the p21-dependent G1 cell cycle arrest. Furthermore, our findings revealed that ANXA13 was negatively regulated by TGF-β/Smad3 signaling as Smad3 could bind to the 3’UTR of ANXA13 and inhibited its transcription, which was confirmed in Smad3 KO mice.
In conclusion, our results demonstrated that ANXA13 is a previously unrecognized protein that functions to protect kidney from AKI. It exerts its protective effect on AKI by directly binding to the TβRI and then inhibiting its phosphorylation, thereby inactivating the TGF-β/Smad3-p21-mediated cell cycle arrest pathway. Thus, ANXA13 may be a novel therapeutic agent for AKI.
