Linking cellular energy state to atrial fibrillation pathogenesis: Potential role of adenosine monophosphate-activated protein kinase

Heart Rhythm. 2020 Aug;17(8):1398-1404. doi: 10.1016/j.hrthm.2020.03.025. Epub 2020 Apr 5.

Abstract

Adenosine monophosphate-activated protein kinase (AMPK) is the cellular stress-sensing molecule. Apart from maintaining cellular energy balance, AMPK controls expression and regulation of ion channels and ion transporters, including cytosolic Ca2+ handling proteins. Emerging evidence suggests that metabolic impairment plays a crucial role in the pathogenesis of atrial fibrillation. AMPK activation is thought to be protective by preventing metabolic stress, favorably modulating membrane electrophysiology including cytosolic Ca2+ dynamics; preventing cellular growth; and hypertrophic remodeling. This review considers current concepts and evidence from clinical and experimental studies regarding the role of AMPK in atrial fibrillation.

Keywords: AF; AMPK; CaTs; DAD.

Publication types

  • Review

MeSH terms

  • AMP-Activated Protein Kinases / metabolism*
  • Animals
  • Atrial Fibrillation / metabolism*
  • Calcium / metabolism
  • Cells, Cultured
  • Energy Metabolism / physiology*
  • Humans
  • Stress, Physiological / physiology*

Substances

  • AMP-Activated Protein Kinases
  • Calcium