Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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) is characterized by progressive renal damage and persistent renal function decline. Renal fibrosis is the critical final common pathway leading to CKD progression. However, the underlying mechanisms and effective therapeutic targets remain poorly understood. Our preliminary data revealed that ubiquitin-specific proteases 43 (USP43) is markedly upregulated in tubular epithelial cells (TECs) from the fibrotic kidneys of human patients and animal models. However, its functional contribution to renal fibrosis has not been elucidated.
Renal tissues from human CKD patients, murine fibrosis models, and HK-2 cells were utilized in this study. The expressions of USP43 in renal fibrosis were evaluated at the protein and RNA levels using western blotting, qRT-PCR and immune staining. To investigate the biological functions and potential targets of USP43, we performed RNA sequencing in both USP43 knockout mice and wild-type control mice after unilateral ureteral obstruction (UUO) treatment, and conducted gain- and loss-of-function experiments in vitro. Immunoprecipitation and ubiquitination assays were performed to investigate the interaction between USP43 and STAT3 and to determine how USP43 regulates STAT3 ubiquitination and degradation.
USP43 expression was significantly elevated in kidneys from CKD patients, as well as in mouse models of renal fibrosis and in TGF-β1-stimulated HK-2 cells. Knockdown of USP43 in HK-2 cells markedly attenuated TGF-β1-induced epithelial injury and fibrotic marker expression. In vivo, USP43 knockdown alleviated renal tubular interstitial fibrosis in both UUO-induced renal injury and streptozotocin (STZ)-induced diabetic kidney injury models. Immunoprecipitation assays confirmed that USP43 directly interacts with STAT3 in TECs. Moreover, USP43 depletion enhanced STAT3 ubiquitination, reduced its protein stability, and consequently alleviated renal fibrogenesis.
These results demonstrated that genetic inhibition of USP43 ameliorates renal fibrosis in CKD by promoting ubiquitination and degradation of STAT3. Targeting USP43 may provide a promising strategies for preventing renal fibrosis and slowing CKD progression.
