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<p>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.</p>

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Targeting STING to disrupt macrophage-mediated adhesion in encapsulating peritoneal sclerosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月23日

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  • Juan Sun,
  • Yuxiang Sun,
  • Dandan Guo,
  • Huolin Ye,
  • Qiang Huang,
  • Hu Zhou,
  • Canming Li,
  • Mei Liao,
  • Yujia You,
  • Hongli Shang,
  • Pan Zhou,
  • Dongxuan Wu,
  • Janusz Witowski,
  • Zhaoyong Hu,
  • Hui Peng

摘要

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.