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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.
Chronic kidney disease (CKD) has high prevalence and mortality rates, and effective interventional drugs are still lacking. The key to preventing and treating CKD lies in mitigating interstitial fibrosis. However, the mechanism by which renal tubular epithelial cells mediate fibroblast activation under injury and stress conditions remains to be elucidated.
The Cullin-RING ubiquitin ligase family is the largest ubiquitin ligase family in mammalian cells, comprising seven members: CUL1 to CUL7. We found that CUL4 expression was significantly increased in the kidneys of the unilateral ureteral obstruction (UUO) model. Knockdown of CUL4 expression in renal tissue significantly aggravated renal fibrosis, suggesting a potential role for CUL4 in inhibiting fibrosis progression. To further explore the mechanism, co-immunoprecipitation combined with mass spectrometry analysis revealed a significant association between CUL4 and the Slit-Robo signaling pathway. Based on these preliminary findings, this study aims to investigate whether CUL4 influences fibroblast activation by regulating the Slit-Robo pathway and its underlying mechanism.
In vivo experiments were conducted using unilateral ureteral obstruction (UUO) and ischemia-reperfusion injury (IRI) mouse models. Techniques included local knockdown, proteomic mass spectrometry, transcriptome/single-cell sequencing, and neutralizing antibody intervention were employed to explore the role of the CUL4-Slit3-Robo signaling axis in renal fibrosis. For in vitro experiments, Slit3 stimulation and Robo1/2 siRNA knockdown were used in fibroblasts to validate the pathway's regulation of cell proliferation and activation.
In both UUO and IRI models, CUL4 expression was upregulated in renal tubular epithelial cells, and its local knockdown exacerbated renal fibrosis. Proteomic mass spectrometry and validation experiments indicated that CUL4 binds to and degrades Slit3. Single-cell sequencing and immunohistochemistry further showed that Slit3 is primarily expressed in renal tubular epithelial cells, while its receptor Robo2 is significantly upregulated in fibroblasts. In vivo, Slit3 neutralizing antibodies alleviated fibrosis. In vitro, Slit3 promoted fibroblast proliferation and activation, an effect that was inhibited by Robo2 knockdown.
During CKD, Slit3 secreted by renal tubular epithelial cells binds to the Robo2 receptor on fibroblasts, promoting fibroblast activation. CUL4 inhibits fibroblast activation and alleviates interstitial fibrosis by degrading Slit3.
