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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.
Diabetes mellitus is a well-established independent risk factor for acute kidney injury (AKI). Diabetic nephropathy (DN), clinically termed diabetic kidney disease (DKD), represents a common complication that significantly elevates the risk of AKI. Additionally, The NOTCH signaling pathway, with particular emphasis on Notch2, has been mechanistically linked to both AKI progression and chronic kidney disease (CKD) development. However, the exact molecular pathways require further elucidation.
Twelve-week-old male BKS db/m (control) and db/db (diabetic) mice underwent bilateral renal ischemia-reperfusion injury (IRI) under anesthesia with 30 min ischemia followed by reperfusion. At 24 hours post-IRI, renal tissues and serum were collected for renal function assessment; histopathology, molecular and serum biomarkers analysis.
In diabetic murine models subjected to renal ischemia-reperfusion injury (IRI), there was a marked exacerbation of renal dysfunction and histopathological damage compared to non-diabetic controls, concomitant with a specific upregulation of Notch2 expression within infiltrating renal macrophages. In vitro experiments further demonstrated that ischemic stress, modeled by hypoxia/reoxygenation, induced Notch2 expression in bone marrow-derived macrophages. Integrative multi-omics analyses of human acute kidney injury datasets and murine single-cell RNA sequencing data identified mitochondrial protein Romo1 as a key downstream effector of Notch2 signaling. Western blot and real-time PCR confirmed that Notch2 signaling upregulates Romo1 expression. Functional investigations revealed that the Notch2- Romo1 axis promotes mitochondrial oxidative stress and sustains M1 macrophage polarization, as evidenced by increased superoxide production and elevated expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), alongside downregulation of M2-associated markers. Importantly, macrophage-specific Notch2 knockdown or inhibition of Romo1 markedly attenuated mitochondrial oxidative damage, reduced inflammatory responses, and ameliorated renal function in diabetic AKI models.
Our findings demonstrate that Notch2 activation in renal macrophages exacerbates diabetic AKI by upregulating Romo1, which drives: Mitochondrial oxidative stress and Sustained M1 macrophage polarization. This Notch2-ROS-M1 axis represents a potential therapeutic target for interrupting the CKD to AKI transition in diabetes.
