What question did this study set out to answer?

This research aims to investigate the relationship between CaMKII activation and remodeling of Ca2+ current in heart failure myocytes.

July 13, 2008Journal of Biological ChemistryOpen Access

Ca2+/Calmodulin-dependent Protein Kinase II-dependent Remodeling of Ca2+ Current in Pressure Overload Heart Failure

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This research aims to investigate the relationship between CaMKII activation and remodeling of Ca2+ current in heart failure myocytes.
Pressure overload heart failure was induced via surgical constriction of the thoracic aorta.
Whole cell patch clamp method was used to record I(Ca) in murine left ventricular myocytes.
CaMKII activity was measured and manipulated to observe effects on I(Ca) density and inactivation.
I(Ca) density was significantly larger in subepicardial myocytes compared to subendocardial myocytes.
In failing left ventricles, I(Ca) density increased in both myocyte types with slowed I(Ca) inactivation (p < 0.05).
CaMKII inhibition reduced I(Ca) density and inactivation time course to control levels, indicating its key role.

Structured PICO

Population

Murine left ventricular (LV) myocytes (subepicardial and subendocardial) from a pressure overload heart failure model induced by surgical constriction of the thoracic aorta

Intervention

CaMKII inhibition by internal diffusion of a specific peptide inhibitor, and internal application of active CaMKII

Comparator

Control myocytes and untreated heart failure myocytes

Outcome

L-type Ca(2+) current (I(Ca)) density and inactivation time coursesurrogate

Activation of CaMKII is a major contributor to pro-arrhythmic L-type Ca2+ current remodeling in load-induced heart failure.

Discussion

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Implication

CaMKII inhibition normalizes I(Ca) remodeling in murine HF; hypothesis-generating for targeted therapy but should not yet change practice.

Cite This Study

Wang et al. (2008) studied this question.

synapsesocial.com/papers/6a7138ca660549caf2c5d96e https://doi.org/10.1074/jbc.m803043200

Topics

Heart failure HFrEF treatment

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Implication

CaMKII inhibition normalizes I(Ca) remodeling in murine HF; hypothesis-generating for targeted therapy but should not yet change practice.

Ca2+/Calmodulin-dependent Protein Kinase II-dependent Remodeling of Ca2+ Current in Pressure Overload Heart Failure

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Topics

Ca2+/Calmodulin-dependent Protein Kinase II-dependent Remodeling of Ca2+ Current in Pressure Overload Heart Failure

Key Points

Structured PICO

Discussion

Implication

Cite This Study

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Topics

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