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Related Experiment Video

Updated: Jul 4, 2026

Mapping Hepatic Stellate Cell Morphology in Mouse Models of Liver Fibrosis
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PNPLA3 I148M Variant Activates Hepatic Stellate Cells via AMIGO2 Upregulation Using iPSC-Derived Model.

Katsuya Toshida1, Kazuki Takeishi1,2, Shinji Itoh1

  • 1Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Liver International : Official Journal of the International Association for the Study of the Liver
|July 3, 2026
PubMed
Summary

A PNPLA3 gene variant promotes liver fibrosis by activating hepatic stellate cells (HSCs) through AMIGO2. This study clarifies the mechanism linking PNPLA3 SNP to liver fibrosis progression.

Keywords:
AMIGO2PNPLA3hepatic stellate cellhuman‐induced pluripotent stem cellsliver fibrosis

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Area of Science:

  • Hepatology
  • Molecular Biology
  • Stem Cell Research

Background:

  • Metabolic-associated fatty liver disease (MAFLD) is linked to a PNPLA3 gene variant.
  • The precise mechanism by which this PNPLA3 single nucleotide polymorphism (SNP) drives liver fibrosis remains unclear.

Purpose of the Study:

  • To elucidate the mechanism of PNPLA3 SNP-induced liver fibrosis.
  • To investigate the role of induced pluripotent stem cell (iPSC)-derived hepatic stellate cells (iHSCs) with the PNPLA3 variant.

Main Methods:

  • Generated iHSCs from iPSCs with either wild-type or variant PNPLA3 (rs73840989).
  • Activated iHSCs using TGF-β1 and analyzed fibrosis markers, growth factors, proliferation, migration, and gene expression via RNA sequencing.
  • Investigated the role of AMIGO2 using siRNA knockdown and assessed epithelial-mesenchymal transition (EMT) markers.

Main Results:

  • Variant-iHSCs showed significantly higher secretion of fibrosis markers (αSMA, COL1A1) and growth factors (PDGF, TGF-β) upon TGF-β1 stimulation.
  • Variant-iHSCs exhibited increased proliferation and migration, with elevated expression of collagen-related genes.
  • AMIGO2 knockdown in variant-iHSCs reduced proliferation and migration, impacting EMT markers (Vimentin, E-cadherin) and decreasing EMT activity and fibrosis protein expression.
  • AMIGO2 protein was detected in PNPLA3-variant liver samples.

Conclusions:

  • The PNPLA3 SNP promotes liver fibrosis through the induction of hepatic stellate cell (HSC) epithelial-mesenchymal transition (EMT).
  • AMIGO2 plays a critical role in mediating the fibrotic effects of the PNPLA3 SNP in HSCs.