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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.
Chronic kidney disease (CKD) and cardiovascular disease (CVD) frequently coexist, posing risks for disease progression. In recent years, the concept of “cardio-renal syndrome” has been proposed, suggesting that disruption of cardio-renal homeostasis mutually exacerbates adverse effects. The renin-angiotensin system, sympathetic nervous system, and inflammation are implicated in the cardio-renal axis. However, the molecular mechanisms remain poorly understood. We have previously reported that a heart failure model (ANS mouse) subjected to simultaneous angiotensin II (A), unilateral nephrectomy (N), and salt administration (S) developed cardiac damages, renal dysfunctions, and proteinuria at 4 weeks post-treatment and may serve as a model for cardio-renal coupling pathophysiology (NOGUCHI K. et al., PNAS, 2020).
The process of urine production in the kidney broadly consists of blood filtration in the glomerulus, followed by secretion and reabsorption in the tubules. When these two structures are impaired, changes in gene expression are expected to differ. However, previous analyses have primarily targeted the whole kidney, the glomerulus specific gene profile has been unknown. Therefore, we incorporated the process of isolating the renal glomerulus into gene expression analysis. Our research objective is to perform more glomerulus-specific analyses and identify factors related to cardio-renal interaction pathologies unique to the renal glomerulus.
ANS treatment was performed on male mice aged 10-12 weeks with a C57Bl/6J background. A control sham-operation group was established simultaneously. After 4 weeks of intervention, hearts and kidneys were harvested from ANS mice. Kidney glomeruli were isolated from the kidneys using the magnetic beads method at the time of harvest. Transcriptome analysis by RNA-Seq was then performed using the heart and renal glomeruli as samples. Weighted Gene Co-expression Network Analysis (WGCNA) was applied to the transcriptome results from each organ to investigate clusters of genes exhibiting similar expression patterns.
In the hearts of ANS mice, pathways such as the Pathogen Induced Cytokine Storm Signaling Pathway and the Pulmonary Fibrosis Idiopathic Signaling Pathway were activated. In the renal glomeruli of ANS mice, pathways such as the Acute Phase Response Signaling Pathway and the Toll-like Receptor Signaling Pathway were activated. A candidate gene cluster of 3318 genes, showing strong correlation between the heart and renal glomeruli, was identified. Using the Matthews Correlation Coefficient; MCC algorithm to analyze interactions between genes in the heart-glomerulus, serotonin receptor-related genes were identified as particularly candidates of strong hub gene.
Our findings uncover a previously unrecognized glomerulus-specific transcriptional network linking heart and kidney pathology. Serotonin receptor–related pathways may serve as a therapeutic target for renal glomerular lesions in cardio-renal syndrome.
