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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 global incidence of Chronic Kidney Disease (CKD) is rising annually, accompanied by a progressive increase in the number of patients with End-Stage Kidney Disease (ESKD) requiring dialysis. Renal fibrosis serves as the converging pathway through which various etiologies of CKD advance to ESKD; however, effective interventions to inhabit this fibrotic process remain elusive.Since macrophage-to-myofibroblast transition(MMT)-derived myofibroblasts constitute 60-85% of the pathogenic α-SMA-positive cells in renal fibrosis (as seen in CKD and UUO models), targeting MMT presents a promising therapeutic approach against this condition.The Annexin A family is a group of important calcium-phospholipid binding proteins. Members such as Annexin A1 and Annexin A3 have been proven to play crucial roles in kidney diseases. This study found that, unlike other family members that are widely expressed in the kidneys, Annexin A13 is mainly specifically expressed in the epithelial cells of renal tubules. Therefore, this prompts us to explore its potential functions in chronic kidney diseases.
To investigate the role of ANXA13, we employed the unilateral ureteral obstruction (UUO) model and achieved renal overexpression of ANXA13 via ultrasound-microbubble-mediated gene delivery.The findings were further confirmed by Western blot, qRT-PCR, and multiplex immunofluorescence. To investigate the mechanism, we performed both single-cell and bulk RNA sequencing.
In the kidney tissue,ANXA13 is primarily expressed in proximal tubular epithelial cells(Figure 1). To investigate its functional role in renal fibrosis, we overexpressed ANXA13 in mouse UUO model. We found that overexpression of ANXA13 markedly alleviated renal fibrosis induced by UUO(Figure 2).Further investigation elucidated that the anti-fibrotic effect of ANXA13 is mediated through the suppression of MMT(Figure 3).
This study demonstrates that ANXA13 overexpression could confers protection against renal fibrosis by suppressing MMT. These findings suggest that ANXA13 could be a promising therapeutic target for treating renal fibrosis and preventing the progression of CKD.
