Protein Kinase Cα Negatively Regulates Systolic and Diastolic Function in Pathological Hypertrophy-Reference-Cited by-同舟云学术

Protein Kinase Cα Negatively Regulates Systolic and Diastolic Function in Pathological Hypertrophy

Published:2003-11-28 Issue:11 Volume:93 Page:1111-1119
ISSN:0009-7330
Container-title:Circulation Research
language:en
Short-container-title:Circulation Research

Author:

Hahn Harvey S.¹,Marreez Yehia¹,Odley Amy¹,Sterbling Amber¹,Yussman Martin G.¹,Hilty K. Chad¹,Bodi Ilona¹,Liggett Stephen B.¹,Schwartz Arnold¹,Dorn Gerald W.¹

Affiliation:

1. From the Departments of Internal Medicine/Cardiology (H.S.H., Y.M., A.O., A.S., M.G.Y., K.C.H., G.W.D.), Institute of Molecular Pharmacology and Biophysics (I.B., A.S.), and Internal Medicine/Pulmonary (S.B.L.), University of Cincinnati Medical Center, Cincinnati, Ohio.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology

Reference40 articles.

1. Targeting the Receptor-G q Interface to Inhibit in Vivo Pressure Overload Myocardial Hypertrophy

2. Absence of pressure overload induced myocardial hypertrophy after conditional inactivation of Gαq/Gα11 in cardiomyocytes

3. Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha 1 adrenergic response.

4. The alpha 1A-adrenergic receptor subtype mediates biochemical, molecular, and morphologic features of cultured myocardial cell hypertrophy

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