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.
Long-term peritoneal dialysis (PD) often leads to peritoneal dysfunction, among which peritoneal fibrosis is particularly common; however, the molecular mechanisms underlying the association between long-term PD induced immune dysregulation and the progression of peritoneal fibrosis remain unclear.
This study integrated multi-omics analyses (including single-cell RNA sequencing and bulk transcriptome sequencing) with experimental validation. An in vitro peritoneal fibrosis model was established by treating human peritoneal mesothelial cells (MeT-5A cells) with transforming growth factor-β1 (TGF-β1). Quantitative real-time polymerase chain reaction (qPCR) and western blot (WB) were used to detect the expression levels of hub genes (S1PR1/S1PR4, namely sphingosine-1-phosphate receptor 1/4) in both cellular samples and clinical samples. The functional role of S1PR4 was verified through gene overexpression and knockdown experiments.
Single-cell sequencing results showed that long-term PD led to a significant decrease in the proportion of natural killer T (NKT) lymphocytes and remodeled the peritoneal immune microenvironment. Integrated transcriptomic analysis further identified S1PR1/S1PR4 as the hub genes closely associated with this process. Experimental validation demonstrated that S1PR1 and S1PR4 were highly expressed in both the peritoneal tissues of patients undergoing long-term PD and in TGF-β1-induced fibrotic cells, and crucially, that modulation of S1PR4 directly regulated fibrosis markers.
This study suggests that, in long-term PD, the dysregulation of the immune microenvironment -characterized by a reduction in NKT cells - may drive the occurrence and progression of peritoneal fibrosis by upregulating the S1PR1/S1PR4 signaling pathways involving S1PR4. It indicates that S1PR1/S1PR4 are potential therapeutic targets for alleviating peritoneal injury and improving the long-term prognosis of PD patients.
