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Cited by 489

The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.

Expression of a β-adrenergic receptor kinase 1 inhibitor prevents the development of myocardial failure in gene-targeted mice

Open access
Rockman, Howard A., Chien, Kenneth R., Choi, Dong-Ju, Iaccarino, Guido, Hunter, John J., Ross, John, Lefkowitz, Robert J., Koch, Walter J.·1998·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.95.12.7000
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Abstract

Heart failure is accompanied by severely impaired β-adrenergic receptor (βAR) function, which includes loss of βAR density and functional uncoupling of remaining receptors. An important mechanism for the rapid desensitization of βAR function is agonist-stimulated receptor phosphorylation by the βAR kinase (βARK1), an enzyme known to be elevated in failing human heart tissue. To investigate whether alterations in βAR function contribute to the development of myocardial failure, transgenic mice with cardiac-restricted overexpression of either a peptide inhibitor of βARK1 or the β 2 AR were mated into a genetic model of murine heart failure ( MLP −/− ). In vivo cardiac function was assessed by echocardiography and cardiac catheterization. Both MLP −/− and MLP −/− /β 2 AR mice had enlarged left ventricular (LV) chambers with significantly reduced fractional shortening and mean velocity of circumferential fiber shortening. In contrast, MLP −/− /βARKct mice had normal LV chamber size and function. Basal LV contractility in the MLP −/− /βARKct mice, as measured by LV dP/dtmax, was increased significantly compared with the MLP −/− mice but less than controls. Importantly, heightened βAR desensitization in the MLP −/− mice, measured in vivo (responsiveness to isoproterenol) and in vitro (isoproterenol-stimulated membrane adenylyl cyclase activity), was completely reversed with overexpression of the βARK1 inhibitor. We report here the striking finding that overexpression of this inhibitor prevents the development of cardiomyopathy in this murine model of heart failure. These findings implicate abnormal βAR-G protein coupling in the pathogenesis of the failing heart and point the way toward development of agents to inhibit βARK1 as a novel mode of therapy.

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Metadata

Authors
Rockman, H. A., Chien, K. R., Choi, D.-J., Iaccarino, G., Hunter, J. J., Ross, J., Lefkowitz, R. J., & Koch, W. J.
Venue
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Published
1998-06-09
Volume
95
Issue
12
Pages
7000-7005
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.95.12.7000
OpenAlex
W2124114189
Cited by
489
References
30
FWCI
15.31
Type
journal article
Language
en
Open access
green

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The paper
Rockman, H. A., Chien, K. R., Choi, D.-J., Iaccarino, G., Hunter, J. J., Ross, J., Lefkowitz, R. J., & Koch, W. J. (1998). Expression of a β-adrenergic receptor kinase 1 inhibitor prevents the development of myocardial failure in gene-targeted mice. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.95.12.7000

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.