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Updated: May 31, 2026

Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
07:46

Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation

Published on: April 3, 2017

mRNA-laden LNP-enabled in situ CAR-macrophage alleviates liver fibrosis via inhibiting activated HSCs and modulating

Xin Huang1, Junfeng Hao1,2, Shuo Wang3

  • 1Department of Family Medicine, Shengjing Hospital of China Medical University, Shenyang 110022, China.

Proceedings of the National Academy of Sciences of the United States of America
|May 29, 2026
PubMed

Insights

This study introduces a novel therapy using liposomal nanoparticles to target liver macrophages, reducing fibrosis by neutralizing activated fibroblasts and promoting liver repair. This approach offers a promising new treatment for liver fibrosis.

Area of Science:

  • Hepatology
  • Immunology
  • Nanomedicine

Background:

  • Liver fibrosis involves excessive extracellular matrix (ECM) deposition, driven by activated hepatic stellate cells (HSCs) and fibroblasts.
  • Fibroblast activation protein (FAP) is crucial in liver fibrosis pathogenesis, making it a key therapeutic target.

Purpose of the Study:

  • To investigate a novel therapeutic strategy for liver fibrosis using FAP-specific CAR-modified macrophages (FAPCAR-M) generated in situ.
  • To evaluate the efficacy of CD163 antibody-conjugated liposomal nanoparticles (LNPs) carrying FAPCAR mRNA in reducing liver fibrosis.

Main Methods:

  • Development of αCD163/LNP-FAPCAR, LNPs designed to deliver FAPCAR mRNA to liver macrophages.
  • In vivo administration of LNPs to induce FAPCAR-M generation and assess their impact on fibrosis markers.

Main Results:

  • LNPs successfully transduced liver macrophages, enhancing their phagocytic activity.
  • Treatment led to significant ECM reduction and improved liver fibrosis resolution.
  • Demonstrated targeted neutralization of hyperactive fibroblasts.

Conclusions:

  • αCD163/LNP-FAPCAR represents a pioneering therapeutic approach for liver fibrosis.
  • In situ generation of FAPCAR-M offers a promising strategy for liver fibrosis management.
  • Targeting FAP-expressing fibroblasts via engineered macrophages shows potential for fibrosis resolution.
Keywords:
ECMFAP-CARLNPsliver fibrosismacrophages

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