Language
English
Publication Date
8-23-2025
Journal
Communications Biology
DOI
10.1038/s42003-025-08662-z
PMID
40847090
PMCID
PMC12373792
PubMedCentral® Posted Date
8-23-2025
PubMedCentral® Full Text Version
Post-print
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.
Keywords
Peritoneal Fibrosis, Animals, Mice, Macrophages, Disease Models, Animal, Membrane Proteins, Signal Transduction, Mice, Inbred C57BL, Cell Adhesion, Chemokine CCL2, Male, Peritoneal Dialysis, Kidney diseases, Peritoneal dialysis
Published Open-Access
yes
Recommended Citation
Sun, Juan; Sun, Yuxiang; Guo, Dandan; et al., "Targeting Sting to Disrupt Macrophage-Mediated Adhesion in Encapsulating Peritoneal Sclerosis" (2025). Faculty and Staff Publications. 4727.
https://digitalcommons.library.tmc.edu/baylor_docs/4727