Calmodulin kinase and L-type calcium channels: A recipe for arrhythmias?

Research output: Contribution to journalArticle

Abstract

L-type Ca2+ channels (LTCCs) are the main portal for Ca 2+ entry into cardiac myocytes. These ion channel proteins open in response to cell membrane depolarizations elicited by action potentials, and LTCC current (ICa) flows during the action potential plateau, to increase cellular Ca2+ (Ca2+i) and trigger myocardial contraction. ICa is also implicated in the genesis of cardiac arrhythmias under conditions such as heart failure and cardiac hypertrophy, in which the action potential plateau and QT interval are prolonged. This article reviews recent findings about the molecular regulation of LTCCs by the Ca2+-dependent signaling molecule, calmodulin kinase II (CaMKII), and compares this form of regulation with regulation by calmodulin-binding domains and β-adrenergic receptor agonists. LTCC dysregulation is discussed in the context of new results showing that CaMKII can be a proarrhythmic signal in disease conditions in which Ca2+i is disordered and cardiac repolarization is excessively prolonged.

Original languageEnglish (US)
Pages (from-to)152-161
Number of pages10
JournalTrends in Cardiovascular Medicine
Volume14
Issue number4
DOIs
StatePublished - May 2004
Externally publishedYes

Fingerprint

L-Type Calcium Channels
Calcium-Calmodulin-Dependent Protein Kinases
Action Potentials
Cardiac Arrhythmias
Cardiomegaly
Myocardial Contraction
Adrenergic Agonists
Calmodulin
Ion Channels
Cardiac Myocytes
Heart Failure
Cell Membrane
Proteins

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Calmodulin kinase and L-type calcium channels : A recipe for arrhythmias? / Anderson, Mark.

In: Trends in Cardiovascular Medicine, Vol. 14, No. 4, 05.2004, p. 152-161.

Research output: Contribution to journalArticle

@article{57fdb8422fa44e57acc4b57a1dfd7719,
title = "Calmodulin kinase and L-type calcium channels: A recipe for arrhythmias?",
abstract = "L-type Ca2+ channels (LTCCs) are the main portal for Ca 2+ entry into cardiac myocytes. These ion channel proteins open in response to cell membrane depolarizations elicited by action potentials, and LTCC current (ICa) flows during the action potential plateau, to increase cellular Ca2+ (Ca2+i) and trigger myocardial contraction. ICa is also implicated in the genesis of cardiac arrhythmias under conditions such as heart failure and cardiac hypertrophy, in which the action potential plateau and QT interval are prolonged. This article reviews recent findings about the molecular regulation of LTCCs by the Ca2+-dependent signaling molecule, calmodulin kinase II (CaMKII), and compares this form of regulation with regulation by calmodulin-binding domains and β-adrenergic receptor agonists. LTCC dysregulation is discussed in the context of new results showing that CaMKII can be a proarrhythmic signal in disease conditions in which Ca2+i is disordered and cardiac repolarization is excessively prolonged.",
author = "Mark Anderson",
year = "2004",
month = "5",
doi = "10.1016/j.tcm.2004.02.005",
language = "English (US)",
volume = "14",
pages = "152--161",
journal = "Trends in Cardiovascular Medicine",
issn = "1050-1738",
publisher = "Elsevier Inc.",
number = "4",

}

TY - JOUR

T1 - Calmodulin kinase and L-type calcium channels

T2 - A recipe for arrhythmias?

AU - Anderson, Mark

PY - 2004/5

Y1 - 2004/5

N2 - L-type Ca2+ channels (LTCCs) are the main portal for Ca 2+ entry into cardiac myocytes. These ion channel proteins open in response to cell membrane depolarizations elicited by action potentials, and LTCC current (ICa) flows during the action potential plateau, to increase cellular Ca2+ (Ca2+i) and trigger myocardial contraction. ICa is also implicated in the genesis of cardiac arrhythmias under conditions such as heart failure and cardiac hypertrophy, in which the action potential plateau and QT interval are prolonged. This article reviews recent findings about the molecular regulation of LTCCs by the Ca2+-dependent signaling molecule, calmodulin kinase II (CaMKII), and compares this form of regulation with regulation by calmodulin-binding domains and β-adrenergic receptor agonists. LTCC dysregulation is discussed in the context of new results showing that CaMKII can be a proarrhythmic signal in disease conditions in which Ca2+i is disordered and cardiac repolarization is excessively prolonged.

AB - L-type Ca2+ channels (LTCCs) are the main portal for Ca 2+ entry into cardiac myocytes. These ion channel proteins open in response to cell membrane depolarizations elicited by action potentials, and LTCC current (ICa) flows during the action potential plateau, to increase cellular Ca2+ (Ca2+i) and trigger myocardial contraction. ICa is also implicated in the genesis of cardiac arrhythmias under conditions such as heart failure and cardiac hypertrophy, in which the action potential plateau and QT interval are prolonged. This article reviews recent findings about the molecular regulation of LTCCs by the Ca2+-dependent signaling molecule, calmodulin kinase II (CaMKII), and compares this form of regulation with regulation by calmodulin-binding domains and β-adrenergic receptor agonists. LTCC dysregulation is discussed in the context of new results showing that CaMKII can be a proarrhythmic signal in disease conditions in which Ca2+i is disordered and cardiac repolarization is excessively prolonged.

UR - http://www.scopus.com/inward/record.url?scp=2942596098&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=2942596098&partnerID=8YFLogxK

U2 - 10.1016/j.tcm.2004.02.005

DO - 10.1016/j.tcm.2004.02.005

M3 - Article

C2 - 15177266

AN - SCOPUS:2942596098

VL - 14

SP - 152

EP - 161

JO - Trends in Cardiovascular Medicine

JF - Trends in Cardiovascular Medicine

SN - 1050-1738

IS - 4

ER -