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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.
Alternative splicing serves as a pivotal RNA processing mechanism that amplifies transcriptomic complexity and proteomic diversity in fibrotic disorders. Emerging evidence underscores the functional significance of RNA-binding protein-regulated splicing variants during fibrogenesis. Staphylococcal nuclease and tudor domain containing 1 gene (SND1) is an RNA-binding protein implicated in extracellular matrix remodeling; however, its regulatory role in peritoneal dialysis (PD)-associated peritoneal fibrosis and the associated splicing circuitry remains mechanistically undefined.
Through analysis of single-cell RNA sequencing data derived from PD patients, we identified SND1 as a hub regulator in fibrogenic niches. Subsequent bulk RNA sequencing with rMATS-mediated alternative splicing profiling deciphered SND1-mediated splicing landscape rewiring. The effects of SND1 on peritoneal mesothelial cell(PMC) senescence and peritoneal fibrosis were detected through a mouse PD model with AAV overexpression or knockdown of SND1 in vivo and in vitro primary PMCs models.
SND1 expression was downregulated in PMCs of peritoneal fibrosis models. Bulk RNA-seq showed that knockdown of SND1 in PMCs predominantly dysregulated pathways related to cellular senescence, cell cycle progression, extracellular matrix synthesis, and inflammatory responses. rMATS analysis of bulk RNA-seq data from SND1-knockdown and control cells identified 153 differential alternative splicing events, with exon skipping being the most prevalent type. Notably, cell division cycle 14B(CDC14B) was identified as a key downstream target of SND1. Reduced SND1 expression induced truncation of exon 2 in CDC14B transcripts, leading to diminished full-length CDC14B protein production, cell cycle arrest in PMCs , and subsequent senescence and peritoneal fibrosis progression. In animal studies, AAV-mediated SND1 overexpression attenuated peritoneal fibrosis, whereas SND1 knockdown exacerbated fibrotic severity.
SND1 in PMCs suppresses cellular senescence and fibrogenesis by regulating CDC14B alternative splicing. This study reveals a novel mechanism underlying PD-associated peritoneal fibrosis and highlights SND1 as a potential therapeutic target for preventing or mitigating peritoneal fibrosis.
The content presented in this abstract was submitted for ASN week 2026 meeting.
