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August 23, 2026Cell Death and DiseaseOpen Access

Targeting HCK in M1 macrophages alleviates postoperative abdominal adhesions by suppressing NF-κB/IL6 axis-driven mesothelial-to-mesenchymal transition

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Authors

ELEnmeng LiTSTianli ShenGLGan Li

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Overview

Preclinical study reveals that targeting HCK suppresses postoperative abdominal adhesions in peritoneal injury models, suggesting a new therapeutic strategy to prevent surgical scarring.

Key Points

  • To determine the role and molecular mechanism of hematopoietic cell kinase (HCK) in M1 macrophage-driven postoperative abdominal adhesion formation.
  • Analyzed HCK expression and macrophage infiltration in peritoneal injury using public databases and in vivo models.
  • Evaluated macrophage polarization, migration, and podosome assembly in vitro following HCK knockout and pharmacological inhibition via Transwell and FITC-gelatin degradation assays.
  • Verified the causal mechanism and therapeutic efficacy using macrophage depletion, adoptive transfer, and perioperative HCK inhibitor administration.
  • HCK deficiency or inhibition suppressed M1 macrophage polarization and eliminated cell migration and invasion by disrupting podosome assembly through NF-κB downregulation.
  • M1 macrophage HCK orchestrated interleukin-6 (IL-6)-driven mesothelial-to-mesenchymal transition (MMT) and myofibroblast differentiation via NF-κB signaling.
  • Perioperative HCK inhibition significantly alleviated postoperative abdominal adhesion formation by preventing MMT-derived myofibroblast accumulation.

Cite This Study

Li et al. (2026) studied this question.

synapsesocial.com/papers/6a8aae407677a34114447199https://doi.org/10.1038/s41419-026-09206-x
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  5. 5Kaempferol Suppresses Mesothelial–Mesenchymal Transition and Attenuates Postoperative Peritoneal Adhesions by Blocking the <scp>TNF</scp>‐α/<scp>COX2</scp> Signalling Pathway2025