ArticleCommunications biology2025
Targeting STING to disrupt macrophage-mediated adhesion in encapsulating peritoneal sclerosis.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
5 citing papers in PubMed.
- Splenic macrophage-B cell axis drives systemic autoimmune-like pathology in Cerebral Malaria.Nature communications · 2026Article
- Article
- The peritoneal immune niche in peritoneal dialysis-induced membrane failure: macrophages, neutrophils and extracellular trap biology.Frontiers in immunology · 2026Review
- Targeting cGAS-STING-macrophage axis: a novel therapeutic horizon for renal fibrosis.Frontiers in immunology · 2026Review
- Macrophage-derived long non-coding RNAs in cancer: pioneering targets for immune modulation and personalized therapy.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Encapsulating peritoneal sclerosis (EPS) is a life-threatening fibrotic condition characterized by severe abdominal adhesions, chronic inflammation, and significant morbidity. The lack of effective treatments for EPS stems from a limited understanding of its underlying mechanisms. In this study, we developed a modified mouse model of PD-induced EPS and investigated the role of the STING signaling pathway in disease progression. Our findings reveal that STING activation in peritoneal mesothelial cells significantly increases the secretion of the macrophage chemokine CCL2, leading to enhanced macrophage infiltration and the formation of pathological adhesions. Notably, pharmacological inhibition of STING using the inhibitor H151 effectively reduced macrophage infiltration and fibrosis, demonstrating its therapeutic potential in alleviating EPS. These results identify the STING pathway as a critical mediator of EPS pathogenesis and suggest that STING inhibitors could offer a promising therapeutic strategy to prevent or reverse EPS, particularly in clinical settings such as peritoneal dialysis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.