Calcium signaling in cardiac ventricular myocytes

Donald M Bers, Tao Guo

Research output: Contribution to journalArticle

122 Scopus citations

Abstract

Calcium (Ca) is a multifunctional regulator of diverse cellular functions. In cardiac muscle Ca is a direct central mediator of electrical activation, ion channel gating, and excitation-contraction (E-C) coupling that all occur on the millisecond time scale. The key amplification step in E-C coupling is under tight control of very local [Ca]. Ca also directly activates signaling via kinases and phosphatases (e.g., Ca-calmodulin-dependent protein kinase [CaMKII] and calcineurin) that occur over a longer time scale (seconds to minutes), and the co-localization of these Ca-dependent modulators to their targets and to Ca is also critical in distinct signaling pathways. Finally, Ca-dependent signaling is also involved in long-term (minutes to hours/days) alterations in gene expression (or excitation-transcription coupling). These pathways are involved in hypertrophy and heart failure, and they can alter the expression of some of the key Ca regulatory proteins involved in E-C coupling and their regulation by kinases and phosphatases. There may again be physical microenvironments involved in this nuclear transcription, such that they sense a discrete Ca signal that is distinct from that involved in E-C coupling. In this way cells can use Ca signaling in multiple ways that function in spatially and temporally distinct manners.

Original languageEnglish (US)
Pages (from-to)86-98
Number of pages13
JournalAnnals of the New York Academy of Sciences
Volume1047
DOIs
StatePublished - 2005
Externally publishedYes

Keywords

  • Calcium
  • Calmodulin
  • Coupling
  • Dependent protein kinase
  • Excitation-contraction coupling

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Fingerprint Dive into the research topics of 'Calcium signaling in cardiac ventricular myocytes'. Together they form a unique fingerprint.

  • Cite this