Atrial remodelling in atrial fibrillation: CaMKII as a nodal proarrhythmic signal

Olurotimi O Mesubi1, Mark E Anderson2

  • 1Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA Department of Medicine, The Johns Hopkins University School of Medicine, 1830 E. Monument Street, Suite 9026, Baltimore, MD 21287, USA.

Cardiovascular Research
|January 15, 2016
PubMed

Insights

Calcium-calmodulin dependent protein kinase II (CaMKII) may promote atrial fibrillation (AF) by affecting various cellular processes. Inhibiting CaMKII shows promise in protecting against AF and correcting calcium handling in human atrial cells.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Calcium-calmodulin dependent protein kinase II (CaMKII) is abundant in heart muscle.
  • Emerging evidence implicates CaMKII in atrial fibrillation (AF) pathogenesis.

Purpose of the Study:

  • To review current evidence on CaMKII's role in AF.
  • To explore CaMKII's molecular targets and therapeutic potential in AF.

Main Methods:

  • Literature review of animal and human studies.
  • Analysis of CaMKII's impact on protein targets related to AF.

Main Results:

  • CaMKII targets proteins involved in membrane excitability, cell survival, calcium homeostasis, matrix remodeling, inflammation, and metabolism.
  • CaMKII inhibition demonstrates protective effects against AF in animal models.
  • CaMKII inhibition corrects defective intracellular calcium handling in human atrial cells.

Conclusions:

  • CaMKII is a significant contributor to AF development and progression.
  • Targeting CaMKII represents a potential therapeutic strategy for managing AF.

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