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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 a disorder characterized by the progressive formation of numerous cysts in the kidneys and liver. It is caused by mutations in the PKD1 or PKD2 genes, leading to defective ciliary function in cystic epithelial cells, resulting in epithelial cell proliferation and cyst fluid retention. The only approved clinical drug for ADPKD is Tolvaptan, a vasopressin V2 receptor (V2R) antagonist that blocks vasopressin signaling, a key driver of cyst growth in ADPKD due to the resulting intracellular increase in cyclic adenosine monophosphate (cAMP). Polyuria is a logical consequence of V2R blockade and is expected to occur in every patient undergoing treatment. This significantly impacts patients' quality of life, prompting the search for novel therapeutic agents for ADPKD.
Using iPS cells from ADPKD patients, Mae et al. successfully generated a collecting duct cyst model. During the establishment of the high-throughput screening (HTS) platform, they found that retinoic acid receptor (RAR) agonists significantly suppressed cyst enlargement. Additionally, in vivo experiments using RAR agonists, TTNPB, and all-trans retinoic acid (ATRA) in both cell cultures and mouse models demonstrated efficacy. This study provided significant inspiration for my research topic.
Tamibarotene, a specific RAR agonist, is a synthetic retinoid drug that has already been approved for relapsed or refractory acute promyelocytic leukemia. Clinical trials of Tamibarotene have already begun in patients with ADPKD, but it is unclear the mechanisms of Tamibarotene. In this study, we investigated the effects of Tamibarotene on renal cyst progression and analyzed their underlying mechanisms using ADPKD model mice.
Pkd1flox/flox: Ksp-Cre mice; an early spontaneous kidney-specific polycystic kidney mouse model. Tamibarotene (5 mg/kg, 10mg/kg) or vehicle was administered by intraperitoneal injection at P3. The mice were sacrificed on postnatal day 9 for analysis. Kidney cyst phenotypes were assessed via kidney-to-body weight ratio (KW/BW) and cyst index (CI, defined as the percentage of cyst area relative to total tissue area). Serum blood urea nitrogen (BUN) levels were measured. For evaluation of cell proliferation, immunohistochemical staining for proliferating cell nuclear antigen (PCNA) was performed.
In the 10mg/kg Tamibarotene group, 2KW/BW and CI were significantly lower than in the other group(2KW/BW: 10.08±2.43%, 9.52±1.17% and 7.86±1.13%, p<0.05. CI: 75.52±4.97%, 72.6±7.07% and 71.02±4.35%, p<0.05. Serum blood urea nitrogen (BUN)showed no significant differences among the three groups. The proportion of Ki-67-positive cells in the kidneys was significantly reduced in the 10 mg/kg group.
Tamibarotene inhibited cyst progression in ADPKD in a dose-dependent manner.
The specific mechanisms will be further investigated.
