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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.
Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequent single-gene disorders. Nevertheless, therapeutic agents for polycystic kidney disease remain limited, and the search for new therapeutic intervention points is essential. The peroxisome is one of the intracellular organelles and is responsible for cellular metabolic functions such as the oxidation of fatty acids and the removal of reactive oxygen species. The interactions with mitochondria have also been increasingly emphasized. It is known that peroxisome proliferator-activated receptor-α (PPARα) activity, a nuclear receptor of peroxisome, is decreased during renal cyst enlargement. Although fenofibrate, a PPARα modulator, has been reported to suppress renal cysts enlargement, it has not yet been applied clinically due to concerns about renal metabolism and nephrotoxicity. In this study, we focused on pemafibrate, a selective PPARα modulator, because its main metabolic pathway is in the liver and is generally considered less likely to cause renal dysfunction. We used this selective PPARα modulator, pemafibrate, to evaluate its effects on renal and hepatic cysts in vitro and in vivo trials.
In vivo study, a mixed diet was prepared using pemafibrate and administered to a cystic kidney rat model (PCK rat). Renal and hepatic functions were evaluated by blood tests in the control and pemafibrate-treated groups, and we evaluated renal cysts and hepatic cysts histologically. We also performed RNA sequencing on each tissue sample. In vitro, we evaluated the effect of pemafibrate on renal cyst enlargement under 3D culture in MDCK2 cells, which is generally used in cystic kidney suppression experiments.
In a rat model of cystic kidney disease, long-term treatment with pemafibrate suppressed the growth of renal cysts and improved renal function. Cyst size reduction was also observed in in vitro 3D culture experiment. RNA sequencing revealed pathway activity patterns characteristic of each tissue.
The favorable effects of pemafibrate in animal models of cystic kidney disease and cellular experiments demonstrated its potential as a clinical treatment for ADPKD. We will evaluate the optimal dosage and toxicity of pemafibrate treatment.
