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Updated: May 12, 2026

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
11:00

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

Published on: September 18, 2017

A Memory Molecule, Ca(2+)/Calmodulin-Dependent Protein Kinase II and Redox Stress; Key Factors for Arrhythmias in a

Young-Hwan Song1

  • 1Department of Pediatrics, Sanggye Paik Hospital, College of Medicine, Inje University, Seoul, Korea.

Korean Circulation Journal
|April 25, 2013
PubMed

Insights

Calcium/calmodulin-dependent protein kinase II (CaMKII) is implicated in heart failure arrhythmias. This enzyme senses intracellular calcium and redox stress, leading to electrical instability and potential sudden cardiac death.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Arrhythmias are common in cardiac diseases like ischemic heart disease and cardiomyopathy.
  • They can worsen heart failure and cause sudden cardiac death.
  • Redox stress and calcium overload are key triggers for arrhythmias in failing hearts.

Purpose of the Study:

  • To review the role of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in heart failure-related arrhythmias.
  • To elucidate the structural and functional properties of CaMKII.
  • To summarize experimental findings on CaMKII interactions with redox stress and ion channels.

Main Methods:

  • Literature review of studies on CaMKII, redox stress, and ion channels in cardiac disease.
  • Analysis of CaMKII's mechanism of activation and sustained function.
  • Synthesis of evidence linking CaMKII to arrhythmogenic processes.

Main Results:

  • CaMKII acts as a central player in heart failure arrhythmias.
  • CaMKII senses intracellular calcium and redox stress.
  • Sustained CaMKII activation, via autophosphorylation or oxidation, contributes to electrical instability.

Conclusions:

  • CaMKII's unique "memory" property enables sustained activation.
  • CaMKII links redox stress and calcium dysregulation to ion channel dysfunction.
  • CaMKII is a potential therapeutic target for preventing arrhythmias in diseased hearts.

Keywords:
Arrhythmias cardiacCalcium-calmodulin-dependent protein kinase type 2Heart failureOxidative stress

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