Evidence of phenotypic alteration as a cause of systolic dysfunction in the failing heart.
This article describes the phenotype of dilated cardiomyopathy in humans and describes parallel studies in experimental models that support or refute the relevance of these changes to the development of the heart failure phenotype.
Feldman
A M
AM
Department of Medicine, University of Pittsburgh School of Medicine, Pennsylvania, USA.
Kubota
T
T
Li
Y Y
YY
Wagner
D
D
Combes
A
A
McTiernan
C
C
D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002311:Cardiomyopathy, Dilated / Q000209:etiology* / Q000503:physiopathology; D019204:GTP-Binding Proteins / Q000378:metabolism; D006321:Heart / Q000503:physiopathology*; D006706:Homeostasis; D006801:Humans; D010641:Phenotype; D011941:Receptors, Adrenergic / Q000502:physiology; D015398:Signal Transduction; D013599:Systole / Q000502:physiology*
D011941:Receptors, Adrenergic; D019204:GTP-Binding Proteins; D000262:Adenylyl Cyclases; D002118:Calcium