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NAG-1/GDF15 modulates hepcidin expression through STAT3 and SMAD pathways.

Pattawika Lertpatipanpong1, Chutwadee Krisanapun2, Kanokkan Boonruang3

  • 1College of Veterinary Medicine and Research Institute for Veterinary Science, Seoul National University, Seoul, 08826, South Korea; Department of Pharmacy Practice, Faculty of Pharmaceutical Sciences, Naresuan University, Phitsanulok, 65000, Thailand.

Archives of Biochemistry and Biophysics
|January 1, 2026
PubMed
Summary

Nonsteroidal Anti-Inflammatory Drug-Activated Gene-1 (NAG-1) suppresses hepcidin expression, a key factor in anemia of inflammation. This study reveals NAG-1

Keywords:
GDF15HepcidinNAG-1SMADSMILESTAT3

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Area of Science:

  • Molecular Biology
  • Endocrinology
  • Iron Metabolism

Background:

  • Hepcidin is a liver hormone regulating iron homeostasis and implicated in anemia of inflammation (AI).
  • Nonsteroidal Anti-Inflammatory Drug-Activated Gene-1 (NAG-1), also known as GDF15, is investigated for its role in hepcidin regulation.

Purpose of the Study:

  • To investigate the regulatory role of NAG-1 in modulating hepcidin expression.
  • To elucidate the molecular mechanisms by which NAG-1 affects hepcidin transcription.

Main Methods:

  • Utilized NAG-1 transgenic mice to assess in vivo effects on hepcidin expression.
  • Established HepG2 cell lines overexpressing wild-type (WT) or mutant NAG-1 (R193A).
  • Analyzed the impact of NAG-1 on IL-6- and BMP6-induced hepcidin expression and signaling pathways (JAK/STAT3, BMP6/SMAD).

Main Results:

  • Elevated circulating NAG-1 in transgenic mice correlated with reduced hepatic hepcidin expression.
  • Both WT and R193A NAG-1 suppressed IL-6- and BMP6-induced hepcidin expression in HepG2 cells.
  • NAG-1 inhibited hepcidin transcription by reducing STAT3 activation and Smad1/5/9 phosphorylation, key components of JAK/STAT3 and BMP6/SMAD pathways.

Conclusions:

  • NAG-1 acts as a negative regulator of hepcidin transcription.
  • The pro-form of NAG-1 possesses significant biological activity in suppressing hepcidin.
  • Findings offer therapeutic insights for managing anemia of inflammation by targeting iron metabolism via NAG-1 modulation.