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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.
Damage-associated molecular patterns (DAMPs) released from injured cells are implicated in chronic inflammation and fibrosis, leading to disease onset. Several studies have reported that extracellular high-mobility group box 1 (HMGB1), one of the major DAMPs, in peritoneal dialysis (PD) effluent promotes peritoneal dysfunction. However, the mechanisms underlying extracellular HMGB1 release from injured cells during PD remain unclear. This study aimed to investigate the involvement of necroptosis, a form of regulated cell death associated with DAMPs release, in peritoneal mesothelial cells (PMCs) on peritoneal dysfunction. In addition, we focused on the cell cycle disturbance as a potential trigger for necroptosis.
The correlation between peritoneal dysfunction and expression of necroptosis-related factors (RIP1, RIP3, MLKL, pMLKL) were analyzed by western blotting using PMCs or supernatants isolated from PD effluent. In vitro, induction of necroptosis and epithelial-mesenchymal transition (EMT) were evaluated by western blotting using omentum-derived PMCs incubated in high glucose medium with or without Necrostatin 2 racemate (Nec-1s: necroptosis inhibitor). Cell cycle was assessed by flow cytometry using high glucose-stimulated PMCs. Additionally, palbociclib (CDK4/6 inhibitor) was administered to examine the effects of suppressing G2/M arrest on necroptosis and EMT in PMCs. In vivo, methylglyoxal-induced peritoneal fibrosis mice (MGO mice) were treated with Nec-1s or palbociclib, and then necroptosis, fibrosis and peritoneal function were evaluated by western blotting analysis, immunohistochemistry and peritoneal equilibration tests.
The upregulation of necroptosis-related factors in PMCs and increased extracellular HMGB1 levels in PD effluent were positively correlated with the severity of peritoneal dysfunction. In vitro, Nec-1s treatment suppressed the high glucose-induced release of HMGB1 and EMT in PMCs. In vivo, Nec-1s reduced HMGB1 levels in ascitic fluid and ameliorated peritoneal function in MGO mice. These data confirmed that high glucose-induced necroptosis contributed to the extracellular release of HMGB1, resulting in peritoneal dysfunction. Further analyses of PD effluent revealed that phosphorylated histone H3 (pHH3), a marker of G2/M phase, positively correlated with upregulation of necroptosis-related factors. Additionally, flow cytometry confirmed an increased proportion of G2/M-arrested cells under high glucose stimulation, and immunofluorescence staining showed co-expression of pHH3 and necroptosis-related factors. Furthermore, reducing the population of G2/M-arrested PMCs using palbociclib suppressed necroptosis and preserved peritoneal function both in vitro and in vivo.
High glucose stimulation induces extracellular release of HMGB1 through the induction of necroptosis in PMCs, resulting in peritoneal dysfunction. Additionally, we confirmed that G2/M arrest in PMCs contributes to the induction of necroptosis. These findings suggest that necroptosis-mediated HMGB1 release and the regulation of cell cycle may represent a potential therapeutic strategy in PD-related peritoneal dysfunction.
