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Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
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Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

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CaMKII in sinoatrial node physiology and dysfunction

Yuejin Wu1, Mark E Anderson2

  • 1Department of Internal Medicine, Carver College of Medicine, University of Iowa Iowa City, IA, USA.

Frontiers in Pharmacology
|March 28, 2014
PubMed

Insights

Calcium and calmodulin-dependent protein kinase II (CaMKII) regulates heart rate responses. Dysfunctional CaMKII contributes to sinoatrial node dysfunction and sudden death.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Electrophysiology

Background:

  • Calcium and calmodulin-dependent protein kinase II (CaMKII) is crucial for sinoatrial node (SAN) pacemaker cell function.
  • CaMKII mediates physiological heart rate acceleration during stress but its role in dysfunction is complex.

Purpose of the Study:

  • To elucidate the role of CaMKII in SAN pacemaking and its contribution to sinoatrial node dysfunction (SND).
  • To investigate how CaMKII activity is regulated by intracellular signals and pathological conditions.

Main Methods:

  • Inhibition of CaMKII in SAN pacemaker cells.
  • Analysis of CaMKII substrate phosphorylation (L-type Ca(2+) channels, phospholamban, RyR2).
  • Assessment of cellular responses to oxidative stress and hyperglycemia.

Main Results:

  • CaMKII inhibition blunts stress-induced heart rate increases without affecting baseline rate.
  • Oxidative modification (ox-CaMKII) leads to constitutive CaMKII activity, promoting SAN cell apoptosis and fibrosis.
  • Excessive CaMKII activity contributes to intracellular calcium overload and reactive oxygen species production.

Conclusions:

  • CaMKII is a key regulator of SAN pacemaker activity and physiological rate adaptation.
  • Pathological CaMKII activation, particularly oxidation, drives SND by causing loss of functional SAN cells.
  • Targeting CaMKII may offer therapeutic strategies for SND.

Keywords:
calciumcalcium/calmodulin-dependent protein kinase IIheart ratesinoatrial nodesinoatrial node dysfunction

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