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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.
The heart and kidneys maintain close physiological crosstalk through the cardiorenal axis, where dysfunction in one organ can instigate or exacerbate dysfunction in the other. This interdependency involves multiple pathological mechanisms, including hemodynamic disturbances, neuroendocrine activation, inflammatory cascades, and metabolic imbalances. In recent years, metabolic reprogramming has garnered significant attention as a potential bridge linking cardiac and renal injury. Studies indicate that metabolic abnormalities in these organs may precede noticeable structural and functional changes. However, the specific metabolic alterations and features of metabolic reprogramming in the kidneys following the onset of heart failure remain unclear.
Using a murine model of chronic cardiac dysfunction induced by transverse aortic constriction (TAC) to mimic left ventricular pressure overload, this study integrated metabolomic, histopathological, and molecular biology analyses to investigate the characteristics of metabolic reprogramming in the heart and kidneys and the dysregulation of ARA metabolism during chronic heart failure development.
(1) Ten weeks post-TAC, mice exhibited significantly reduced LVEF and LVFS, accompanied by ventricular hypertrophy and dilation. Renal tissues showed inflammatory infiltration and mild fibrosis, though serum creatinine levels were unchanged. (2) Untargeted metabolomics revealed distinct metabolic perturbations in cardiac and renal tissues post-heart failure, with KEGG pathway enrichment highlighting glycerophospholipid and ARA metabolism as the most disrupted. Targeted validation confirmed elevated levels of ARA and its downstream metabolites in both organs. (3) Western blot and immunohistochemistry demonstrated upregulated cPLA2α expression in cardiorenal tissues, alongside renal tubular accumulation of ACSL4 and 4-HNE, implicating ARA release and lipid peroxidation in renal injury following heart failure.
This study delineates cardiorenal metabolic reprogramming following chronic cardiac insufficiency and elucidates both shared and organ-specific dysregulation in ARA metabolism. cPLA2α-mediated ARA release and subsequent inflammatory and lipid peroxidation cascades contribute to cardiorenal crosstalk, providing a theoretical foundation for multi-organ protective strategies targeting the ARA metabolic pathway.
