Phosphoinositide 3-kinase γ-deficient mice are protected from isoproterenol-induced heart failure

We have recently shown that genetic inactivation of phosphoinositide 3-kinase gamma (PI3Kgamma), the isoform linked to G-protein-coupled receptors, results in increased cardiac contractility with no effect on basal cell size. Signaling via the G-protein-coupled beta-adrenergic receptors has been imp...

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Veröffentlicht in:	Circulation (New York, N.Y.) N.Y.), 2003-10, Vol.108 (17), p.2147-2152
Hauptverfasser:	OUDIT, Gavin Y, CRACKOWER, Michael A, STEINBERG, Susan F, BACKX, Peter H, PENNINGER, Josef M, ERIKSSON, Urs, SARAO, Renu, KOZIERADZKI, Ivona, SASAKI, Takehiko, IRIE-SASAKI, Junko, GIDREWICZ, Dominica, RYBIN, Vitalyi O, WADA, Teiji
Format:	Artikel
Sprache:	eng
Schlagworte:	Adrenergic beta-Agonists Animals Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cardiomegaly - chemically induced Cardiomegaly - enzymology Cardiomegaly - prevention & control Catalytic Domain - genetics Disease Models, Animal Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Fibrosis - genetics Fibrosis - pathology Fibrosis - prevention & control Heart - drug effects Heart Failure - chemically induced Heart Failure - enzymology Heart Failure - pathology Heart Failure - prevention & control Isoproterenol Male Medical sciences Mice Mice, Knockout Myocardium - enzymology Myocardium - pathology Phosphatidylinositol 3-Kinases - deficiency Phosphatidylinositol 3-Kinases - genetics Signal Transduction - drug effects Signal Transduction - genetics
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