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Fibroblast Growth Factor 1 Reduces Pulmonary Vein and Atrium Arrhythmogenesis via Modification of Oxidative Stress

Yen-Yu Lu1,2, Chen-Chuan Cheng3, Shih-Yu Huang2,4,5

  • 1Division of Cardiology, Department of Internal Medicine, Sijhih Cathay General Hospital, New Taipei City, Taiwan.

Frontiers in Cardiovascular Medicine
|February 4, 2022
PubMed

Insights

Fibroblast growth factor (FGF) 1 demonstrates anti-arrhythmic potential by improving calcium (Ca2+) homeostasis and reducing oxidative stress in pulmonary vein and left atrium myocytes. This study investigated FGF1

Area of Science:

  • Cardiology
  • Molecular Biology
  • Electrophysiology

Background:

  • Atrial fibrillation (AF) poses a significant health burden, with calcium (Ca2+) dysregulation and oxidative stress as key contributors.
  • Fibroblast growth factor (FGF) 1 possesses known antioxidant properties and the ability to modulate Ca2+ homeostasis.

Purpose of the Study:

  • To investigate the anti-arrhythmic potential of FGF1.
  • To determine if FGF1 modulates Ca2+ homeostasis and antioxidant activity in pulmonary vein (PV) and left atrium (LA) myocytes.

Main Methods:

  • Electrophysiological recordings using patch clamp and conventional microelectrodes in isolated rabbit PV and LA myocytes and tissue preparations.
  • Assessment of cellular and mitochondrial oxidative stress.
  • Western blotting and confocal microscopy were employed.

Main Results:

  • FGF1 treatment in rabbits led to slower heart rates and prolonged action potential duration in PV and LA tissues.
  • FGF1 reduced oxidative stress and Ca2+ transients in PV and LA myocytes.
  • FGF1 modulated specific ionic currents (INa-L, Ito, IKr-tail) in a manner dependent on the Protein Kinase C (PKC)ε pathway.

Conclusions:

  • FGF1 exhibits anti-arrhythmic properties by altering electrophysiological characteristics of PV and LA myocytes.
  • The observed effects are likely mediated through modulation of oxidative stress, Ca2+/Na+ homeostasis, and the PKCε signaling pathway.
Abstract

Keywords:
atrial fibrillationcalcium regulationfibroblast growth factor 1oxidative stresspulmonary vein

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