Calmodulin kinase signaling in heart: An intriguing candidate target for therapy of myocardial dysfunction and arrhythmias

Mark E. Anderson

doi:10.1016/j.pharmthera.2004.11.002

Calmodulin kinase signaling in heart: An intriguing candidate target for therapy of myocardial dysfunction and arrhythmias

Mark E. Anderson

Research output: Contribution to journal › Review article › peer-review

108 Scopus citations

Abstract

The multifunctional Ca²⁺/calmodulin (CaM)-dependent protein kinase II (CaMKII) has emerged as a proarrhythmic and procardiomyopathic signal in a wide range of structural heart diseases. This review discusses CaMKII structure and function and recent evidence implicating CaMKII inhibition as a potential strategy for treating myocardial dysfunction and arrhythmias in the setting of structural heart disease.

Original language	English (US)
Pages (from-to)	39-55
Number of pages	17
Journal	Pharmacology and Therapeutics
Volume	106
Issue number	1
DOIs	https://doi.org/10.1016/j.pharmthera.2004.11.002
State	Published - Apr 2005
Externally published	Yes

Keywords

Arrhythmia
Calmodulin kinase
Cellular calcium
Electrophysiology
Structural heart disease
Sudden death

ASJC Scopus subject areas

Pharmacology
Pharmacology (medical)

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10.1016/j.pharmthera.2004.11.002

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title = "Calmodulin kinase signaling in heart: An intriguing candidate target for therapy of myocardial dysfunction and arrhythmias",

abstract = "The multifunctional Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) has emerged as a proarrhythmic and procardiomyopathic signal in a wide range of structural heart diseases. This review discusses CaMKII structure and function and recent evidence implicating CaMKII inhibition as a potential strategy for treating myocardial dysfunction and arrhythmias in the setting of structural heart disease.",

keywords = "Arrhythmia, Calmodulin kinase, Cellular calcium, Electrophysiology, Structural heart disease, Sudden death",

author = "Anderson, {Mark E.}",

note = "Funding Information: This work was supported by grants from the National Institutes of Health (HL62494, HL70250, and HL46681). Dr. Anderson is an established investigator for the American Heart Association.",

year = "2005",

month = apr,

doi = "10.1016/j.pharmthera.2004.11.002",

language = "English (US)",

volume = "106",

pages = "39--55",

journal = "Pharmacology and Therapeutics",

issn = "0163-7258",

publisher = "Elsevier Inc.",

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TY - JOUR

T1 - Calmodulin kinase signaling in heart

T2 - An intriguing candidate target for therapy of myocardial dysfunction and arrhythmias

AU - Anderson, Mark E.

N1 - Funding Information: This work was supported by grants from the National Institutes of Health (HL62494, HL70250, and HL46681). Dr. Anderson is an established investigator for the American Heart Association.

PY - 2005/4

Y1 - 2005/4

N2 - The multifunctional Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) has emerged as a proarrhythmic and procardiomyopathic signal in a wide range of structural heart diseases. This review discusses CaMKII structure and function and recent evidence implicating CaMKII inhibition as a potential strategy for treating myocardial dysfunction and arrhythmias in the setting of structural heart disease.

AB - The multifunctional Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) has emerged as a proarrhythmic and procardiomyopathic signal in a wide range of structural heart diseases. This review discusses CaMKII structure and function and recent evidence implicating CaMKII inhibition as a potential strategy for treating myocardial dysfunction and arrhythmias in the setting of structural heart disease.

KW - Arrhythmia

KW - Calmodulin kinase

KW - Cellular calcium

KW - Electrophysiology

KW - Structural heart disease

KW - Sudden death

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DO - 10.1016/j.pharmthera.2004.11.002

M3 - Review article

C2 - 15781121

AN - SCOPUS:15244345086

SN - 0163-7258

VL - 106

SP - 39

EP - 55

JO - Pharmacology and Therapeutics

JF - Pharmacology and Therapeutics

IS - 1

ER -

Calmodulin kinase signaling in heart: An intriguing candidate target for therapy of myocardial dysfunction and arrhythmias

Abstract

Keywords

ASJC Scopus subject areas

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