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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.
Diabetic kidney disease (DKD) represents the leading cause of chronic kidney disease globally, with cellular senescence, particularly in tubular epithelial cells, emerging as a key contributor to its pathogenesis. The polyphenolic compound Procyanidin C1 (PCC1) has demonstrated senotherapeutic potential in various aging-related contexts, however, its specific effects and mechanism in DKD remain unexplored. This study aimed to investigate the protective role of PCC1 against diabetes-induced renal tubular senescence and injury and to elucidate its underlying molecular pathways.
The role of PCC1 against diabetes-induced tubular senescence and injury was evaluated in vitro in tubular epithelial cells and in murine models of streptozotocin-elicited DKD.
In vitro in tubular epithelial cells, PCC1 treatment significantly mitigated diabetic milieu-induced “cellular senescence” and “P53 pathway signaling”, as identified by KEGG analysis of RNA-sequencing data. Specifically, PCC1 attenuated senescence markers, including reduced γH2AX foci formation, decreased senescence-associated-β-galactosidase activity, and downregulated expression of key mediators of senescence signaling like p16INK4A and p21. These effects were associated with suppressed phosphorylation of p53 at Ser15, a key event in the senescence cascade that can be activated by reactive oxygen species (ROS). Mechanistically, PCC1 targeted the active site pocket of arginase-II (Arg-II), inhibiting its enzyme activity and subsequently reducing ROS production and p53 phosphorylation at Ser15. Notably, forced expression of Arg-II abolished the senotherapeutic effect of PCC1, confirming Arg-II as its critical molecular target. In murine models of streptozotocin-elicited DKD, PCC1 therapy inhibited Arg-II expression and p53 phosphorylation in tubular cells, leading to reduced tubular senescence and injury, along with improved diabetes-induced renal injury.
These findings highlight PCC1 as a novel senotherapeutic agent that attenuates DKD progression by targeting the Arg-II/ROS/p53 pathway, offering a promising strategy for DKD management.
