Calmodulin kinase II inhibition protects against structural heart disease

β-Adrenergic receptor (βAR) stimulation increases cytosolic Ca 2+ to physiologically augment cardiac contraction, whereas excessive βAR activation causes adverse cardiac remodeling, including myocardial hypertrophy, dilation and dysfunction, in individuals with myocardial infarction. The Ca 2+ -calm...

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Veröffentlicht in:	Nature medicine 2005-04, Vol.11 (4), p.409-417
Hauptverfasser:	Zhang, Rong, Khoo, Michelle S C, Wu, Yuejin, Yang, Yingbo, Grueter, Chad E, Ni, Gemin, Price, Edward E, Thiel, William, Guatimosim, Silvia, Song, Long-Sheng, Madu, Ernest C, Shah, Anisha N, Vishnivetskaya, Tatiana A, Atkinson, James B, Gurevich, Vsevolod V, Salama, Guy, Lederer, W J, Colbran, Roger J, Anderson, Mark E
Format:	Artikel
Sprache:	eng
Schlagworte:	Adrenergic beta-Antagonists - pharmacology Animals Arrhythmias, Cardiac - metabolism Biomedical and Life Sciences Biomedicine Biophysics Calcium - metabolism Calcium-Calmodulin-Dependent Protein Kinase Type 2 Calcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitors Calcium-Calmodulin-Dependent Protein Kinases - physiology Cancer Research Cardiac Output, Low Cardiomegaly Cardiovascular disease Cardiovascular diseases Heart attacks Infectious Diseases Inhibition Kinases Medicine Metabolic Diseases Mice Mice, Transgenic Molecular Medicine Myocardial Contraction Myocardial infarction Myocardial Infarction - metabolism Myocardial Infarction - physiopathology Neurosciences Peptides Phosphorylation Physiology Protein expression Proteins Transgenic animals Ventricular Remodeling
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