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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) caused by ischemia–reperfusion injury (IRI) remains a major clinical challenge. Platelet activation contributes to post-ischemic inflammation, but the specific role of the ADP receptor P2Y12, central to platelet activation, has not been fully clarified. This study aimed to investigate whether P2Y12 promotes renal injury through platelet-mediated inflammation and to explore its downstream mechanisms.
A unilateral renal IRI model was established in C57BL/6 wild-type (WT) and P2Y12 global knockout (KO) mice. Kidney function was evaluated by serum creatinine (sCr). Tubular damage was assessed by histological scoring of H&E and PAS-stained sections. Gene expression of platelet activation markers (Pf4, Ccl5, Selp), adhesion molecules (Icam1, Vcam1), pro-inflammatory cytokines (Il1b, Il6, Tnf), and immune cell markers (F4/80, Ly6g) was measured by quantitative real-time PCR (qRT-PCR). Protein expression and phosphorylation of PI3K and Akt were examined by Western blotting, and localization of P2Y12, ICAM-1, VCAM-1, F4/80, and Ly6G was analyzed by immunohistochemistry.
P2Y12 expression was markedly increased in the kidney after IRI. Compared with WT controls, P2Y12-deficient mice exhibited significantly lower sCr levels at 72 h after reperfusion and reduced tubular necrosis. Renal expression of the injury marker NGAL was also decreased. Deletion of P2Y12 significantly reduced mRNA levels of platelet activation markers and endothelial adhesion molecules, indicating attenuated platelet and endothelial activation. Inflammatory cytokines and immune cell markers were down-regulated in the kidneys of P2Y12-KO mice, accompanied by fewer macrophage and neutrophil infiltrates on histological staining. Furthermore, Western blot analysis revealed that phosphorylation of PI3K and Akt was substantially suppressed in P2Y12-deficient kidneys after IRI, suggesting that P2Y12 promotes inflammatory injury via PI3K/Akt signaling.
P2Y12 plays a critical role in the pathogenesis of ischemia–reperfusion–induced AKI by facilitating platelet activation, endothelial adhesion, and inflammatory cell recruitment through the PI3K/Akt pathway. Genetic deletion of P2Y12 confers significant protection against renal dysfunction and tissue injury. These findings provide experimental evidence that targeting P2Y12 may represent a promising therapeutic strategy to alleviate inflammation and improve outcomes in AKI.
