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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.
Previous studies have demonstrated that patients with chronic kidney disease (CKD) who also suffer from periodontitis are at an increased risk of renal function decline. However, the mechanisms underlying CKD progression induced by periodontitis remain poorly understood. Recently, advanced ‘-omics’ methodologies have been introduced, offering the potential to uncover complex molecular mechanisms. In this study, we aimed to identify the signaling changes in the kidney following the induction of periodontitis in mice using next-generation sequencing approaches.
Experiments were conducted using a folic acid-induced CKD mouse model (FAN-CKD) and a ligature-induced periodontitis mouse model (LIG). Kidney function was assessed through blood sampling, and periodontal tissue was evaluated using micro-computed tomography (μCT). Kidney samples were further analyzed using Western blotting and RNA sequencing (RNA-seq) to identify molecular pathways responsible for the exacerbation of kidney damage caused by periodontitis. For cell culture experiments, human renal tubular epithelial cells (HK-2 cells) were used.
In the FAN-CKD group, kidney function was significantly worsened by the induction of periodontitis via ligature. Furthermore, μCT imaging confirmed that ligature induced periodontitis with consistent severity. RNA-seq analysis comparing FAN vs. FAN+LIG showed the upregulation of interferon (IFN) alpha/beta signaling, including IRF7, STAT1, and ISG20, and a strong upregulation of beta-catenin signaling, and downregulation of AMPK signals in the kidney following ligature treatment. The upregulation of beta-catenin signaling target genes was also found in the FAN-CKD model in comparison to the control. Western blot analysis showed decreased phosphorylation of beta-catenin at the Ser552 site, which is known to inactivate beta-catenin activity. A 24-hour incubation with IFN-gamma in HK-2 cells showed inhibition of phosphorylation of AMPK at the Thr 172 site and CTNNB1 (beta-catenin) at the Ser 552 site.
The progression of CKD induced by periodontitis is associated with the activation of beta-catenin signaling, which is known to play a role in the transition from acute kidney injury (AKI) to CKD. IFN-gamma-induced activation of CTNNB1 suggests a role for the IFN signal in periodontitis-induced kidney disease progression. These findings suggest that shared signaling alterations may play a pivotal role in the pathophysiological connection between periodontitis and CKD.
