Ca2+/calmodulin-dependent protein kinase II in heart failure

Howard Schulman; Mark E. Anderson

doi:10.1016/j.ddmec.2010.07.005

Ca²⁺/calmodulin-dependent protein kinase II in heart failure

Howard Schulman, Mark E. Anderson

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

16 Scopus citations

Abstract

Ca²⁺/calmodulin (CaM)-dependent protein kinase II (CaMKII) is now recognized to play a central role in myocardial biology and disease. CaMKII appears to grade myocardial performance and regulate heart rate by catalyzing the phosphorylation of major proteins involved in cardiac excitation-contraction coupling. Under pathological stress, CaMKII activates hypertrophic and inflammatory transcriptional pathways and promotes apoptosis. Animal studies suggest that CaMKII inhibition may be an effective approach for treating common forms of structural heart disease.

Original language	English (US)
Pages (from-to)	e117-e122
Journal	Drug Discovery Today: Disease Mechanisms
Volume	7
Issue number	2
DOIs	https://doi.org/10.1016/j.ddmec.2010.07.005
State	Published - Jun 2010
Externally published	Yes

ASJC Scopus subject areas

Molecular Medicine
Drug Discovery

Access to Document

10.1016/j.ddmec.2010.07.005

Cite this

@article{731c1bd806a34be6b5e4fb8d413a2efa,

title = "Ca2+/calmodulin-dependent protein kinase II in heart failure",

abstract = "Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) is now recognized to play a central role in myocardial biology and disease. CaMKII appears to grade myocardial performance and regulate heart rate by catalyzing the phosphorylation of major proteins involved in cardiac excitation-contraction coupling. Under pathological stress, CaMKII activates hypertrophic and inflammatory transcriptional pathways and promotes apoptosis. Animal studies suggest that CaMKII inhibition may be an effective approach for treating common forms of structural heart disease.",

author = "Howard Schulman and Anderson, {Mark E.}",

note = "Funding Information: This work was supported in part by the Fondation Leducq Alliance for CaMKII Signaling in Heart Disease (Grant 08CVD01) and by NIH Grants R01HL70250, R01HL079031, and R01HL096652.",

year = "2010",

month = jun,

doi = "10.1016/j.ddmec.2010.07.005",

language = "English (US)",

volume = "7",

pages = "e117--e122",

journal = "Drug Discovery Today: Disease Mechanisms",

issn = "1740-6765",

publisher = "Elsevier Limited",

number = "2",

}

TY - JOUR

T1 - Ca2+/calmodulin-dependent protein kinase II in heart failure

AU - Schulman, Howard

AU - Anderson, Mark E.

N1 - Funding Information: This work was supported in part by the Fondation Leducq Alliance for CaMKII Signaling in Heart Disease (Grant 08CVD01) and by NIH Grants R01HL70250, R01HL079031, and R01HL096652.

PY - 2010/6

Y1 - 2010/6

N2 - Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) is now recognized to play a central role in myocardial biology and disease. CaMKII appears to grade myocardial performance and regulate heart rate by catalyzing the phosphorylation of major proteins involved in cardiac excitation-contraction coupling. Under pathological stress, CaMKII activates hypertrophic and inflammatory transcriptional pathways and promotes apoptosis. Animal studies suggest that CaMKII inhibition may be an effective approach for treating common forms of structural heart disease.

AB - Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) is now recognized to play a central role in myocardial biology and disease. CaMKII appears to grade myocardial performance and regulate heart rate by catalyzing the phosphorylation of major proteins involved in cardiac excitation-contraction coupling. Under pathological stress, CaMKII activates hypertrophic and inflammatory transcriptional pathways and promotes apoptosis. Animal studies suggest that CaMKII inhibition may be an effective approach for treating common forms of structural heart disease.

UR - http://www.scopus.com/inward/record.url?scp=78649263331&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78649263331&partnerID=8YFLogxK

U2 - 10.1016/j.ddmec.2010.07.005

DO - 10.1016/j.ddmec.2010.07.005

M3 - Review article

C2 - 21503275

AN - SCOPUS:78649263331

SN - 1740-6765

VL - 7

SP - e117-e122

JO - Drug Discovery Today: Disease Mechanisms

JF - Drug Discovery Today: Disease Mechanisms

IS - 2

ER -

Ca²⁺/calmodulin-dependent protein kinase II in heart failure

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this