Anti-beta(1)-adrenergic receptor antibodies and heart failure: causation, not just correlation.
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2004-05
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Abstract
Antibodies specific for the beta(1)-adrenergic receptor are found in patients with chronic heart failure of various etiologies. From work presented in this issue of the JCI, we can now infer that these antibodies actually contribute to the pathogenesis of chronic heart failure. This commentary discusses mechanisms by which these antibodies may engender cardiomyopathy.
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Freedman, Neil J, and Robert J Lefkowitz (2004). Anti-beta(1)-adrenergic receptor antibodies and heart failure: causation, not just correlation. J Clin Invest, 113(10). pp. 1379–1382. 10.1172/JCI21748 Retrieved from https://hdl.handle.net/10161/5930.
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Neil J. Freedman
Our work focuses on atherosclerosis-related signal transduction and the genetic bases of atherosclerosis and vein graft failure, both in vitro and in vivo. We investigate the regulation of receptor protein tyrosine kinases by G protein-coupled receptor kinases (GRKs), and the role of GRKs and β-arrestins in atherosclerosis; molecular mechanisms of atherogenesis associated with the dual Rho-GEF kalirin, the F-actin-binding protein Drebrin, and small nucleolar RNAs (snoRNAs) of the Rpl13a locus. For in vivo modeling of atherosclerosis and neointimal hyperplasia, we use mouse carotid artery bypass grafting with either veins or arteries from gene-deleted or congenic wild type mice, as well as aortic atherosclerosis studies and bone marrow transplantation. To study receptor phosphorylation, signal transduction, and intracellular trafficking, we employ primary smooth muscle cells, endothelial cells, and macrophages derived from knockout mice, as well as cells treated with RNA interference.
Key Words: atherosclerosis, G protein-coupled receptor kinases, arrestins, desensitization, phosphorylation, receptor protein tyrosine kinases, smooth muscle cells, neointimal hyperplasia, Rho-GEF, Drebrin, snoRNAs.
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