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Updated: Oct 21, 2025

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Fibroblast growth factor 21 inhibited inflammation and fibrosis after myocardial infarction via EGR1

Jiamin Li1, Liling Gong1, Ruijie Zhang1

  • 1Department of Pharmacology, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Medicine Research, Ministry of Education, Harbin Medical University, Harbin, 150081, China.

European Journal of Pharmacology
|September 3, 2021
PubMed

Insights

Fibroblast growth factor 21 (FGF21) reduces cardiac inflammation and fibrosis after heart attack. FGF21 works by regulating the FGFR-EGR1 pathway, improving heart remodeling and function.

Area of Science:

  • Cardiovascular Biology
  • Regenerative Medicine
  • Molecular Cardiology

Background:

  • Myocardial fibrosis following myocardial infarction (MI) contributes to adverse ventricular remodeling.
  • Fibroblast growth factor 21 (FGF21) is implicated in cardiovascular and metabolic diseases, but its role in post-MI cardiac inflammation and fibrosis is unclear.

Purpose of the Study:

  • To investigate the therapeutic effects of FGF21 on cardiac inflammation and fibrosis post-MI.
  • To elucidate the underlying molecular mechanisms of FGF21 action in the injured heart.

Main Methods:

  • Adult male Sprague-Dawley rats underwent MI and were treated with recombinant human basic FGF21 (rhbFGF21).
  • Cardiac function was assessed via echocardiography.
  • Cardiac inflammation and fibrosis were evaluated using histological staining (hematoxylin-eosin and Masson's trichrome).
  • The role of FGF receptors (FGFRs) and the early growth response protein 1 (EGR1) pathway was examined.

Main Results:

  • rhbFGF21 administration improved cardiac function and reduced cardiac inflammation and fibrosis.
  • FGF21 treatment led to decreased expression of inflammatory and fibrosis-related factors.
  • Blocking FGFRs abolished the beneficial effects of FGF21.
  • Oxidative stress-induced downregulation of EGR1 was identified as a key mechanism, contributing to reduced inflammation and fibrosis.

Conclusions:

  • FGF21 effectively suppresses cardiac inflammation and fibrosis in post-MI hearts.
  • The therapeutic effects of FGF21 are mediated through the FGFR-EGR1 signaling pathway.
  • FGF21 represents a potential therapeutic target for mitigating adverse cardiac remodeling after myocardial infarction.

Keywords:
EGR1FGF21InflammationMyocardial fibrosis

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