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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.
Cisplatin is a widely used chemotherapeutic agent for solid tumors, but its cumulative nephrotoxicity often progresses to chronic kidney disease (CKD). Although the mechanisms underlying cisplatin-induced acute kidney injury have been extensively studied, the cellular responses leading to chronic fibrosis remain poorly understood. In this study, we established a clinically relevant in vitro model of CKD by repeatedly exposing rat kidney fibroblasts (NRK-49F) to low-dose cisplatin (RLDC).
Compared with single high-dose cisplatin (SHDC) exposure, RLDC induced persistent fibroblast-to-myofibroblast transformation, as shown by elevated α-smooth muscle actin (α-SMA) and fibronectin expression. Morphological analysis revealed pronounced cellular hypertrophy, including increased cell surface area, nuclear size, and cell volume. RLDC also upregulated p21 and senescence-associated β-galactosidase activity, indicating the development of a senescence phenotype. Flow cytometry demonstrated that RLDC-treated fibroblasts were arrested at the G2/M phase, linking cell cycle arrest to senescence and myofibroblast activation. Inhibition of p21 significantly reduced RAC-induced hypertrophy, senescence, and α-SMA expression, confirming its essential role in this process. Mechanistically, repeated cisplatin exposure activated Yes-associated protein (YAP), a transcriptional regulator known to drive tissue fibrosis. Disruption of the YAP–TEAD interaction using Verteporfin markedly attenuated RLDC-induced cellular hypertrophy, senescence, and myofibroblast transformation.
Together, these results suggest that repeated low-dose cisplatin induces fibroblast-to-myofibroblast transition through YAP activation and G2/M arrest–associated p21 signaling.
This study highlights cellular senescence as a key pathological link between chronic injury and fibrotic remodeling and identifies YAP and p21 as potential therapeutic targets to prevent cisplatin-induced CKD.
