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Related Experiment Video

Updated: Feb 20, 2026

Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo
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RIPK3 Orchestrates Scar-Associated Macrophage Dysfunction to Drive Pulmonary Fibrosis.

Tao Yang1,2, Xiao Li1,2, Shuyue Lei1,2

  • 1State Key Laboratory of Chemical Biology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|February 19, 2026
PubMed
Summary

Receptor-interacting protein kinase 3 (RIPK3) regulates pulmonary fibrosis by controlling macrophage metabolism, independent of cell death. Targeting this pathway offers a potential therapeutic strategy for idiopathic pulmonary fibrosis (IPF).

Keywords:
IPFRIPK3SAMsSPP1arginine metabolism

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Area of Science:

  • Immunology
  • Cell Biology
  • Metabolism

Background:

  • Idiopathic pulmonary fibrosis (IPF) involves abnormal tissue remodeling and immune system dysfunction.
  • Receptor-interacting protein kinase 3 (RIPK3) is known for its role in necroptosis, but its non-necroptotic functions in fibrosis are unclear.

Purpose of the Study:

  • To investigate the non-necroptotic functions of RIPK3 in pulmonary fibrosis.
  • To identify the role of RIPK3 in regulating macrophage function and metabolism during fibrosis.

Main Methods:

  • Analysis of RIPK3 expression in IPF patients and mice.
  • Generation and analysis of macrophage-specific RIPK3 knockout mice.
  • Bleomycin-induced lung fibrosis model.
  • Single-cell RNA sequencing.
  • In vitro differentiation and functional analysis of scar-associated macrophages (SAMs).

Main Results:

  • RIPK3 is upregulated in IPF and enriched in macrophages.
  • Macrophage-specific RIPK3 knockout mice showed resistance to bleomycin-induced fibrosis.
  • RIPK3 regulates SAMs and their pro-fibrotic functions.
  • RIPK3 deficiency in SAMs inhibits arginine-to-polyamine conversion via the AKT-mTOR pathway, reducing pro-fibrotic polyamine accumulation.

Conclusions:

  • RIPK3 has a distinct, necroptosis-independent immunometabolic role in pulmonary fibrosis.
  • RIPK3 acts as a key metabolic regulator within the fibrotic niche by influencing SAMs.
  • Targeting the RIPK3-mediated immunometabolic axis presents a potential therapeutic strategy for IPF.