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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.
Salvador family WW domain-containing protein 1 (SAV1) is an important component of the Hippo signaling pathway, which plays a key role in organ development and tissue homeostasis. Disruption of this pathway has been associated with various diseases, including those related to aging. Kidney ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) and often progresses to chronic kidney disease (CKD), particularly in older individuals. This study investigated whether protein kinase B (AKT) is involved in the kidney restoration process regulated by SAV1 following IRI.
A proximal tubule-specific SAV1 knockout in the kidneys (SAV1ptKO) was generated, and both wild-type (WT) and SAV1ptKO mice underwent kidney IRI or sham operation. The mice were then treated with MK-2206, an AKT inhibitor, or vehicle control. Kidney function was evaluated by measuring plasma creatinine and blood urea nitrogen levels. Tubular injury and cell proliferation were assessed using histological techniques, including periodic acid-Schiff stating and immunohistochemistry. Additionally, western blot analysis was performed to examine proteins associated with cell proliferation.
Forty-eight hours after IRI, SAV1ptKO mice exhibited impaired kidney function, whereas WT mice showed significant recovery. Consistent with the functional data, tubular histological damage in the cortex by kidney IRI was significantly reduced 48 hours after IRI in WT mice, but remained severe in SAV1ptKO mice. Similarly, 48 hours after IRI, the number of Ki67-positive cells in the cortex was higher in WT mice than SAV1ptKO mice. AKT activation was markedly increased in SAV1ptKO mice compared to WT mice 48 hours after IRI. Pharmacological inhibition of AKT improved kidney function and reduced tubular histological damage induced by IRI in SAV1ptKO mice.
These findings indicate that SAV1 deficiency in proximal tubules delays kidney restoration after IRI by promoting AKT activation.
