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Experimental antiarrhythmic targets: CaMKII inhibition - ready for clinical evaluation?

Lars S Maier1

  • 1Abt. Kardiologie und Pneumologie / Herzzentrum, Deutsches Zentrum fur Herzkreislaufforschung, Georg-August-Universitat Gottingen, Robert-Koch-Str. 40 37075 Gottingen, Germany. lmaier@med.uni-goettingen.de.

Current Medicinal Chemistry
|July 19, 2013
PubMed

Insights

Calcium/calmodulin-dependent protein kinase II (CaMKII) plays a role in heart failure and arrhythmias. Inhibiting CaMKII may be a future therapeutic strategy for these cardiac conditions.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is increasingly implicated in cardiac hypertrophy, heart failure, and arrhythmias.
  • Both animal models and human studies suggest a link between CaMKII activity and cardiac dysfunction.

Purpose of the Study:

  • To elucidate the role of CaMKII in excitation-contraction coupling.
  • To highlight CaMKII-dependent proarrhythmogenic mechanisms, specifically SR Ca(2+) leak and late Na(+) current.

Main Methods:

  • Review of existing literature on CaMKII in cardiac function and arrhythmias.
  • Focus on mechanisms involving sarcoplasmic reticulum (SR) Ca(2+) leak and late Na(+) current.

Main Results:

  • CaMKII is a key mediator in cardiac excitation-contraction coupling.
  • CaMKII activation contributes to proarrhythmogenic events through SR Ca(2+) leak and enhanced late Na(+) current.

Conclusions:

  • CaMKII plays a significant role in cardiac arrhythmias.
  • CaMKII inhibition presents a potential future therapeutic strategy for managing cardiac arrhythmias and heart failure.

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