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Calcium, calmodulin, and calcium-calmodulin kinase II: heartbeat to heartbeat and beyond

Lars S Maier1, Donald M Bers

  • 1Department of Physiology, Stritch School of Medicine, Loyola University-Chicago, 2160 South First Avenue, Chicago, IL 60153, USA.

Journal of Molecular and Cellular Cardiology
|September 18, 2002
PubMed

Insights

Calcium (Ca) regulates cardiac contraction via excitation-contraction coupling. Calmodulin (CaM) and Ca-CaM-dependent kinase II (CaMKII) also modulate this process and excitation-transcription coupling in heart failure.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Physiology

Background:

  • Calcium (Ca) is central to cardiac excitation-contraction (E-C) coupling.
  • Dysregulation of E-C coupling is implicated in cardiac hypertrophy and heart failure.
  • Ca-dependent proteins, notably calmodulin (CaM) and Ca-CaM-dependent kinase II (CaMKII), influence cellular Ca handling.

Purpose of the Study:

  • To review the established role of Ca in E-C coupling.
  • To explore the modulatory functions of CaM and CaMKII in E-C coupling.
  • To examine the contribution of Ca, CaM, and CaMKII to excitation-transcription (E-T) coupling in pathological conditions.

Main Methods:

  • Literature review of Ca signaling in cardiac function.
  • Analysis of the roles of CaM and CaMKII in ion channel and transporter modulation.
  • Investigation of Ca-dependent signaling pathways in cardiac hypertrophy and heart failure.

Main Results:

  • Ca influx and sarcoplasmic reticulum (SR) Ca release/uptake are critical in E-C coupling.
  • CaM and CaMKII directly impact Ca influx, SR Ca handling, and associated proteins.
  • These Ca-dependent pathways contribute to both acute Ca handling and longer-term E-T coupling.

Conclusions:

  • CaM and CaMKII are key modulators of cardiac E-C coupling.
  • Alterations in Ca, CaM, and CaMKII signaling are significant in heart failure.
  • Understanding these pathways is crucial for addressing cardiac dysfunction.

Keywords:
Non-programmatic

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