Role of Ca2+/calmodulin-dependent protein kinase (CaMK) in excitation-contraction coupling in the heart

Lars S. Maier, Donald M Bers

Research output: Contribution to journalArticle

200 Citations (Scopus)

Abstract

Calcium (Ca2+) is the central second messenger in the translation of electrical signals into mechanical activity of the heart. This highly coordinated process, termed excitation-contraction coupling or ECC, is based on Ca2+-induced Ca2+ release from the sarcoplasmic reticulum (SR). In recent years it has become increasingly clear that several Ca2+-dependent proteins contribute to the fine tuning of ECC. One of these is the Ca2+/calmodulin-dependent protein kinase (CaMK) of which CaMKII is the predominant cardiac isoform. During ECC CaMKII phosphorylates several Ca2+ handling proteins with multiple functional consequences. CaMKII may also be co-localized to distinct target proteins. CaMKII expression as well as activity are reported to be increased in heart failure and CaMKII overexpression can exert distinct and novel effects on ECC in the heart and in isolated myocytes of animals. In the present review we summarize important aspects of the role of CaMKII in ECC with an emphasis on recent novel findings.

Original languageEnglish (US)
Pages (from-to)631-640
Number of pages10
JournalCardiovascular Research
Volume73
Issue number4
DOIs
StatePublished - Mar 1 2007
Externally publishedYes

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Calcium-Calmodulin-Dependent Protein Kinase Type 2
Excitation Contraction Coupling
Calcium-Calmodulin-Dependent Protein Kinases
Proteins
Sarcoplasmic Reticulum
Second Messenger Systems
Muscle Cells
Protein Isoforms
Heart Failure
Calcium

Keywords

  • Calcium
  • Calmodulin
  • CaM kinase
  • E-C coupling
  • Heart

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Role of Ca2+/calmodulin-dependent protein kinase (CaMK) in excitation-contraction coupling in the heart. / Maier, Lars S.; Bers, Donald M.

In: Cardiovascular Research, Vol. 73, No. 4, 01.03.2007, p. 631-640.

Research output: Contribution to journalArticle

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