ArticleProceedings of the National Academy of Sciences of the United States of America1997
Restoration of beta-adrenergic signaling in failing cardiac ventricular myocytes via adenoviral-mediated gene transfer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 193 citations in OpenAlex.
- G-protein receptor kinases 2, 5 and 6 redundantly modulate Smoothened-GATA transcriptional crosstalk in fetal mouse hearts.Journal of molecular and cellular cardiology · 2018Article
- Promise of adeno-associated virus as a gene therapy vector for cardiovascular diseases.Heart failure reviews · 2017Review
- Pathological hypertrophy reverses β2-adrenergic receptor-induced angiogenesis in mouse heart.Physiological reports · 2015Article
- GRK2 in the heart: a GPCR kinase and beyond.Antioxidants & redox signaling · 2014Review
- G-protein βγ subunit dimers modulate kidney repair after ischemia-reperfusion injury in rats.Molecular pharmacology · 2014Article
- Cardiovascular gene therapy for myocardial infarction.Expert opinion on biological therapy · 2014Review
- Molecular targeting of Gα and Gβγ subunits: a potential approach for cancer therapeutics.Trends in pharmacological sciences · 2013Review
- New advances in beta-blocker therapy in heart failure.Frontiers in physiology · 2013Review
- G protein-coupled receptor kinases in normal and failing myocardium.Frontiers in bioscience (Landmark edition) · 2011Review
- GRK2 as a novel gene therapy target in heart failure.Journal of molecular and cellular cardiology · 2011Review
- The inotropic peptide βARKct improves βAR responsiveness in normal and failing cardiomyocytes through G(βγ)-mediated L-type calcium current disinhibition.Circulation research · 2011Article
- Reversal of impaired myocardial beta-adrenergic receptor signaling by continuous-flow left ventricular assist device support.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2010Article
- Uncoupling of myocardial beta-adrenergic receptor signaling during coronary artery bypass grafting: the role of GRK2.The Annals of thoracic surgery · 2008Article
- Central role of Gq in the hypertrophic signal transduction of angiotensin II in vascular smooth muscle cells.Endocrinology · 2008Article
- Gene therapy in heart failure.Circulation research · 2008Review
- Alveolar epithelial beta2-adrenergic receptors.American journal of respiratory cell and molecular biology · 2008Review
- Beta-adrenergic receptor signaling in cardiac function and heart failure.McGill journal of medicine : MJM : an international forum for the advancement of medical sciences by students · 2007Article
- Crosstalk between Gi and Gq/Gs pathways in airway smooth muscle regulates bronchial contractility and relaxation.The Journal of clinical investigation · 2007Article
- Genetic and phenotypic targeting of β-adrenergic signaling in heart failure.Molecular and cellular biochemistry · 2004Article
- Regulation of cardiac contractility by Rab4-modulated beta2-adrenergic receptor recycling.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Cardiovascular gene therapy is a novel approach to the treatment of diseases such as congestive heart failure (CHF). Gene transfer to the heart would allow for the replacement of defective or missing cellular proteins that may improve cardiac performance. Our laboratory has been focusing on the feasibility of restoring beta-adrenergic signaling deficiencies that are a characteristic of chronic CHF. We have now studied isolated ventricular myocytes from rabbits that have been chronically paced to produce hemodynamic failure. We document molecular beta-adrenergic signaling defects including down-regulation of myocardial beta-adrenergic receptors (beta-ARs), functional beta-AR uncoupling, and an up-regulation of the beta-AR kinase (betaARK1). Adenoviral-mediated gene transfer of the human beta2-AR or an inhibitor of betaARK1 to these failing myocytes led to the restoration of beta-AR signaling. These results demonstrate that defects present in this critical myocardial signaling pathway can be corrected in vitro using genetic modification and raise the possibility of novel inotropic therapies for CHF including the inhibition of betaARK1 activity in the heart.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.