ArticleJournal of cellular and molecular medicine2019
ST2 blockade mitigates peritoneal fibrosis induced by TGF-β and high glucose.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Effects of finerenone on arterial stiffness and cardiorenal biomarkers in patients with type 2 diabetes and chronic kidney disease: a randomised placebo-controlled mechanistic trial (FIVE-STAR).Cardiovascular diabetology · 2025Trial
- sST2 is a key outcome biomarker in COVID-19: insights from discovery randomized trial.Scientific reports · 2025Trial
- Peritoneal Dialysis -Associated Fibrosis: Emerging Mechanisms and Therapeutic Opportunities.Frontiers in pharmacology · 2025Review
- Osteoprotegerin and Inflammation in Incident Peritoneal Dialysis Patients.Journal of clinical medicine · 2024Article
- A review of research progress on mechanisms of peritoneal fibrosis related to peritoneal dialysis.Frontiers in physiology · 2023Review
- Loss of JNK-Associated Leucine Zipper Protein Promotes Peritoneal Dialysis-Related Peritoneal Fibrosis.Kidney diseases (Basel, Switzerland) · 2022Article
- Saikosaponin D Inhibits Peritoneal Fibrosis in Rats With Renal Failure by Regulation of TGFβ1/ BMP7 / Gremlin1/ Smad Pathway.Frontiers in pharmacology · 2021Article
- ST2 blockade mitigates peritoneal fibrosis induced by TGF-β and high glucose.Journal of cellular and molecular medicine · 2019Article
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peritoneal fibrosis (PF) is an intractable complication of peritoneal dialysis (PD) that leads to peritoneal membrane failure. This study investigated the role of suppression of tumorigenicity (ST)2 in PF using patient samples along with mouse and cell-based models. Baseline dialysate soluble (s)ST2 level in patients measured 1 month after PD initiation was 2063.4 ± 2457.8 pg/mL; patients who switched to haemodialysis had elevated sST2 levels in peritoneal effluent (1576.2 ± 199.9 pg/mL, P = .03), which was associated with PD failure (P = .04). Baseline sST2 showed good performance in predicting PD failure (area under the receiver operating characteristic curve = 0.780, P = .001). In mice with chlorhexidine gluconate-induced PF, ST2 was expressed in fibroblasts and mesothelial cells within submesothelial zones. In primary cultured human peritoneal mesothelial cells (HPMCs), transforming growth factor-β treatment increased ST2, fibronectin, β-galactosidase and Snail protein levels and decreased E-cadherin level. Anti-ST2 antibody administration reversed the up-regulation of ST2 and fibronectin expression; it also reduced fibrosis induced by high glucose (100 mmol/L) in HPMCs. Thus, high ST2 level in dialysate is a marker for fibrosis and inflammation during peritoneal injury, and blocking ST2 may be an effective therapeutic strategy for renal preservation.
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