CaMKII and a failing strategy for growth in heart.

Abstract

Patients with systolic left ventricular dysfunction die progressively from congestive heart failure or die suddenly from cardiac arrhythmias. Myocardial hypertrophy is an early event in most forms of heart failure, but the majority of patients with myocardial hypertrophy do not develop heart failure. Developing improved therapies for targeting the cell signaling pathways that enable this deadly transition from early myocardial insult to heart failure and sudden death is a key goal for improving public health. In this issue of the JCI, Ling and colleagues provide new evidence that activation of the multifunctional Ca(2+)/calmodulin-dependent kinase IIdelta is a decisive step on the path to heart failure in mice (see the related article beginning on page 1230).

• Authors: Mark E Anderson
• Journal: The Journal of clinical investigation (J Clin Invest) Vol. 119 Issue 5 Pg. 1082-5 (May 2009) ISSN: 1558-8238 [Electronic] United States
• PMID: 19422097 (Publication Type: Comment, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• Protein Isoforms
• protein kinase D
• Protein Kinase C
• Calcium-Calmodulin-Dependent Protein Kinase Type 2

Topics

• Animals
• Calcium-Calmodulin-Dependent Protein Kinase Type 2 (antagonists & inhibitors, physiology)
• Cardiomegaly (complications, metabolism, pathology)
• Heart (physiopathology)
• Heart Failure (complications, drug therapy, pathology, physiopathology)
• Humans
• Mice
• Models, Biological
• Myocardium (metabolism, pathology)
• Phosphorylation
• Protein Isoforms (physiology)
• Protein Kinase C (metabolism)
• Ventricular Dysfunction, Left (complications, physiopathology)