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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.
Macrophage is educated by the tubule epithelial cell with maladaptive repair during the renal maladaptive repair, which is one of the most important characteristic features in acute kidney injury (AKI) to chronic kidney disease (CKD) transition. However, the underlying mechanism of orchestrating characterization of macrophage in renal maladaptive repair remains largely unclear. This study investigated the role of macrophage metabolic reprogramming in maladaptive repair and delineated the contribution of the NF-κB–HIF-1α axis in AKI to CKD transition.
Bilateral ischemia–reperfusion injury (I/RI) and unilateral ureteral obstruction (UUO) models were used to establish AKI to CKD transition in C57BL/6J mice. Kidney function, histopathology, and fibrosis markers were assessed. Macrophage infiltration and phenotype were analyzed by immunohistochemistry, Western blotting, and qPCR. Macrophage depletion was performed with clodronate liposomes. To investigate molecular mechanisms, myeloid-specific HIF-1α knockout mice and the NF-κB inhibitor BAY11-7082 were employed in vivo, while in vitro studies included co-culture of TECs and bone marrow–derived macrophages under prolonged hypoxia–reoxygenation. Glycolysis was modulated with 2-deoxy-D-glucose, and chromatin immunoprecipitation combined with database analysis was used to confirm transcriptional regulation of HIF-1α by NF-κB.
Both I/RI and UUO models exhibited impaired recovery with tubular injury and interstitial fibrosis. These changes were accompanied by marked macrophage infiltration and enrichment of a pro-inflammatory phenotype characterized by iNOS and Mincle expression as well as increased TNF-α, IL-1β, and MCP-1. Macrophage depletion markedly reduced fibrosis and improved renal outcomes. Glycolysis was enhanced in macrophages during AKI to CKD transition, with increased hexokinase activity, lactate, and pyruvate levels. Pharmacological inhibition of glycolysis attenuated the pro-inflammatory phenotype and inflammatory cytokine production. Mechanistic studies revealed that HIF-1α expression was increased in macrophages, driving glycolysis and maintaining pro-inflammatory phenotype. Myeloid HIF-1α knockout significantly reduced glycolytic activity, suppressed inflammatory phenotype, and ameliorated fibrosis in both I/RI and UUO models. Furthermore, NF-κB directly bound the HIF-1α promoter and transcriptionally upregulated its expression. Inhibition of NF-κB reduced HIF-1α expression, impaired glycolytic metabolism, suppressed pro-inflammatory phenotype, and alleviated renal fibrosis and functional decline in vivo.
These findings identify pro-inflammatory macrophages as key drivers of maladaptive renal repair through HIF-1α–mediated glycolytic reprogramming. The NF-κB–HIF-1α signaling axis governs this process and represents a critical pathogenic pathway in AKI to CKD transition. Targeting macrophage metabolism by disrupting NF-κB–HIF-1α signaling provides a promising therapeutic strategy to mitigate maladaptive repair and slow CKD progression following AKI.
