DukeSpace Home
→
Duke Faculty Scholarship
→
Browsing Duke Faculty Scholarship by Duke-affiliated Author

Browsing Duke Faculty Scholarship by Duke-affiliated Author "Koch, Walter J."

Now showing items 1-9 of 9

Alterations in cardiac adrenergic signaling and calcium cycling differentially affect the progression of cardiomyopathy

Lefkowitz, Robert J.; Iaccarino, Guido; Koch, Walter J. (American Society for Clinical Investigation, 2001-04)

The medical treatment of chronic heart failure has undergone a dramatic transition in the past decade. Short-term approaches for altering hemodynamics have given way to long-term, reparative strategies, including ...
Catecholamines, Cardiac β-Adrenergic Receptors, and Heart Failure

Lefkowitz, Robert J.; Rockman, Howard Allan; Koch, Walter J. (American Heart Association, 2000-04)
Enhancement of cardiac function after adenoviral-mediated in vivo intracoronary β2-adrenergic receptor gene delivery

Maurice, John; Hata, Jonathan Andrew; Shah, Ashish; White, David Cloid; McDonald, Patricia; Dolber, Paul Christian; Wilson, Katrina; Lefkowitz, Robert J.; Glower, Donald D. Jr.; Koch, Walter J. (American Society for Clinical Investigation, 1999-07)

Exogenous gene delivery to alter the function of the heart is a potential novel therapeutic strategy for treatment of cardiovascular diseases such as heart failure (HF). Before gene therapy approaches to alter cardiac ...
G Protein Signaling and Vein Graft Intimal Hyperplasia: Reduction of Intimal Hyperplasia in Vein Grafts by a Gbg Inhibitor

Davies, Mark; Huynh, Tam; Fulton, Gregory; Lefkowitz, Robert J.; Hagen, Per-Otto Frode; Koch, Walter J. (American Heart Association, 1998-08)

Abstract—Vein grafting results in the development of intimal hyperplasia with accompanying changes in guanine nucleotide–binding (G) protein expression and function. Several serum mitogens that act through G protein–coupled ...
Hybrid Transgenic Mice Reveal In Vivo Specificity of G Protein–Coupled Receptor Kinases in the Heart

Eckhart, Andrea Dawn; Duncan, Sandra; Lefkowitz, Robert J.; Koch, Walter J. (American Heart Association, 2000-01)

G protein–coupled receptor kinases (GRKs) phosphorylate activated G protein-coupled receptors, including α1B-adrenergic receptors (ARs), resulting in desensitization. In vivo analysis of GRK substrate selectivity has been ...
In Vivo Inhibition of Elevated Myocardial β-Adrenergic Receptor Kinase Activity in Hybrid Transgenic Mice Restores Normal β-Adrenergic Signaling and Function

Akhter, Shahab; Eckhart, Andrea Dawn; Shotwell, Kyle; Lefkowitz, Robert J.; Koch, Walter J. (American Heart Association, 1999-08)

Background Stimulation of β1- and β2-adrenergic receptors (ARs) in the heart results in positive inotropy. In contrast, it has been reported that the β3AR is also expressed in the human heart and that its stimulation leads ...
In Vivo Ventricular Gene Delivery of a β-Adrenergic Receptor Kinase Inhibitor to the Failing Heart Reverses Cardiac Dysfunction

Shah, Ashish; White, David Cloid; Emani, Sitaram; Kypson, Alan; Lilly, R. Eric; Wilson, Katrina; Glower, Donald D. Jr.; Lefkowitz, Robert J.; Koch, Walter J. (American Heart Association, 2001-03)

Background—Genetic manipulation to reverse molecular abnormalities associated with dysfunctional myocardium may provide novel treatment. This study aimed to determine the feasibility and functional consequences of in vivo ...
Reciprocal In Vivo Regulation of Myocardial G Protein-Coupled Receptor Kinase Expression by b-Adrenergic Receptor Stimulation and Blockade

Lefkowitz, Robert J.; Koch, Walter J.; Tomhave, Eric; Iaccarino, Guido (American Heart Association, 1998)

Background—Impaired myocardial β-adrenergic receptor (βAR) signaling, including desensitization and functional uncoupling, is a characteristic of congestive heart failure. A contributing mechanism for this impairment may ...
β-Adrenergic Receptor Kinase-1 Levels in Catecholamine-Induced Myocardial Hypertrophy

Iaccarino, Guido; Dolber, Paul Christian; Lefkowitz, Robert J.; Koch, Walter J. (American Heart Association, 1999-01)

Pressure overload ventricular hypertrophy is accompanied by dysfunctional β-adrenergic receptor signaling due to increased levels of the β-adrenergic receptor kinase-1, which phosphorylates and desensitizes β-adrenergic ...