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March 7, 2015AJP Heart and Circulatory PhysiologyOpen Access

Chasing cardiac physiology and pathology down the CaMKII cascade

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Key result

CaMKII regulates fundamental proteins involved in cardiac excitation-contraction coupling, and its dysregulation constitutes a central mechanism in cardiac diseases like ischemia/reperfusion injury, arrhythmias, and hypertrophy.

Authors

AMAlicia MattiazziRBRosana A. BassaniAEAriel L. Escobar

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Overview

CaMKII dysregulation merits mechanistic study in cardiac disease; extends conceptual framework but leaves open targeted clinical translation.

PICO

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Population
Cardiac physiology and pathology

This review provides a conceptual framework for understanding the central role of the CaMKII cascade in cardiac physiology and various cardiac pathologies.

Cite This Study

Mattiazzi et al. (2015) conducted a review in Cardiac physiology and pathology. CaMKII regulates fundamental proteins involved in cardiac excitation-contraction coupling, and its dysregulation constitutes a central mechanism in cardiac diseases like ischemia/reperfusion injury, arrhythmias, and hypertrophy.

synapsesocial.com/papers/6a158b1ad64fa333899fcaachttps://doi.org/10.1152/ajpheart.00007.2015
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Also Consider

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  1. 1Effects of pH on Na+-Ca2+ exchange in canine cardiac sarcolemmal vesicles.1982 · 245 citations
  2. 2The stunned myocardium: prolonged, postischemic ventricular dysfunction.1982 · 2,812 citations
  3. 3CaMKIIdelta subtypes: localization and function2014 · 86 citations
  4. 4Ca2+–calmodulin‐dependent protein kinase II represses cardiac transcription of the L‐type calcium channel α1C‐subunit gene (Cacna1c) by DREAM translocation2011 · 73 citations
  5. 5The Nuclear δB Isoform of Ca2+/Calmodulin-dependent Protein Kinase II Regulates Atrial Natriuretic Factor Gene Expression in Ventricular Myocytes1997 · 212 citations