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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.
The development of kidney organoids derived from human induced pluripotent stem cells (iPSCs) represents a major advance in modeling kidney pathophysiology and disease progression. However, iPSC-derived kidney organoids largely reflect the fetal kidney and show limited capacity to reproduce age-related and senescence-associated phenotypes that are pivotal in chronic kidney disease (CKD). Considering that cellular senescence plays a key role in the transition from acute kidney injury (AKI) to CKD, there is a strong need for models that can capture this process under human-relevant conditions. To overcome this limitation, we established an artificial cellular aging and CKD model that closely mimics the human in vivo environment by repeatedly administering cisplatin to renal tubular organoids (tubuloids) derived from primary human proximal tubular epithelial cells (hRPTECs) cultured from explanted human kidneys.
Tubuloids derived from explanted kidneys were characterized by RNA sequencing to define their cellular composition. Repeated exposure to cisplatin was applied to induce progressive cellular senescence. Expression of senescence markers was analyzed by Western blotting, immunofluorescence staining, and flow cytometry. Fibrosis-related changes were assessed using fibrosis bioassay, cell migration assay, and collagen gel contraction assay. Inflammatory cytokine expression and secretion were evaluated through immunohistochemistry and quantitative PCR to determine the activation of the senescence-associated secretory phenotype (SASP).
The generated tubuloids consisted predominantly of proximal tubular cells, accounting for over 60% of the total population. Cisplatin treatment elevated markers of DNA damage response (γH2AX), epithelial injury (KIM-1), and apoptosis (caspase-3). Repeated administration markedly increased the proportion of cells arrested in the G2/M phase and upregulated senescence markers including p16 and p21. Furthermore, secretion of inflammatory cytokines, indicative of SASP activation, was significantly enhanced. Conditioned media from cisplatin-treated tubuloids promoted proliferation, differentiation, migration, and contraction of myofibroblasts, suggesting the release of pro-fibrotic cytokines mediated by SASP factors.
We established a reproducible cisplatin-induced tubuloid model that recapitulates key pathological features of CKD, including epithelial senescence, SASP activation, inflammation, and fibrosis. This model bridges the gap between in vitro systems and human kidney pathophysiology and provides a promising alternative to animal models, which have limited translational predictability. Our human tubuloid platform offers new opportunities for studying CKD mechanisms and for screening anti-fibrotic and senescence-modifying therapeutics relevant to the AKI-to-CKD transition.
