ReviewJournal of cardiovascular translational research2010
betaARKct: a therapeutic approach for improved adrenergic signaling and function in heart disease.
Review in Journal of cardiovascular translational research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Arrestins as Possible Drug Targets.Biomolecules & therapeutics · 2025Review
- Isoproterenol pre-treatment improve the therapeutic efficacy of cardiosphere-derived cells transplantation for myocardial infarction.Journal of thoracic disease · 2023Article
- Novel roles for G protein-coupled receptor kinases in cardiac injury and repair.Biochemical Society transactions · 2023Review
- GRK2 in cardiovascular disease and its potential as a therapeutic target.Journal of molecular and cellular cardiology · 2022Review
- Effect of β-adrenergic receptor kinase inhibitor on post-myocardial infarction heart failure in rats.International journal of clinical and experimental pathology · 2017Article
- PAQR3 regulates Golgi vesicle fission and transport via the Gβγ-PKD signaling pathway.Cellular signalling · 2015Article
- Alterations in reversible protein histidine phosphorylation as intracellular signals in cardiovascular disease.Frontiers in pharmacology · 2015Review
- A needleless liquid jet injection delivery method for cardiac gene therapy: a comparative evaluation versus standard routes of delivery reveals enhanced therapeutic retention and cardiac specific gene expression.Journal of cardiovascular translational research · 2014Article
- GRK 2 level in peripheral blood lymphocytes of elderly patients with acute myocardial infarction.Journal of geriatric cardiology : JGC · 2013Article
- Heart failure gene therapy: the path to clinical practice.Circulation research · 2013Review
- Prodeath signaling of G protein-coupled receptor kinase 2 in cardiac myocytes after ischemic stress occurs via extracellular signal-regulated kinase-dependent heat shock protein 90-mediated mitochondrial targeting.Circulation research · 2013Article
- AAV6-βARKct gene delivery mediated by molecular cardiac surgery with recirculating delivery (MCARD) in sheep results in robust gene expression and increased adrenergic reserve.The Journal of thoracic and cardiovascular surgery · 2012Article
- Conducting the G-protein Coupled Receptor (GPCR) Signaling Symphony in Cardiovascular Diseases: New Therapeutic Approaches.Drug discovery today. Disease models · 2012Article
- AAV vectors for cardiac gene transfer: experimental tools and clinical opportunities.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Review
- G protein coupled receptor kinases as therapeutic targets in cardiovascular disease.Circulation research · 2011Review
- G protein-coupled receptor kinases in normal and failing myocardium.Frontiers in bioscience (Landmark edition) · 2011Review
- Targeting G protein-coupled receptor kinases (GRKs) in Heart Failure.Drug discovery today. Disease mechanisms · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the most powerful regulators of cardiovascular function is catecholamine-stimulated adrenergic receptor (AR) signaling. The failing heart is characterized by desensitization and impaired beta-AR responsiveness as a result of upregulated G protein-coupled receptor kinase-2 (GRK2) present in injured myocardium. Deterioration of cardiac function is progressively enhanced by chronic adrenergic over-stimulation due to increased levels of circulating catecholamines. Increased GRK2 activity contributes to this pathological cycle of over-stimulation but lowered responsiveness. Over the past two decades the GRK2 inhibitory peptide betaARKct has been identified as a potential therapy that is able to break this vicious cycle of self-perpetuating deregulation of the beta-AR system and subsequent myocardial malfunction, thus halting development of cardiac failure. The betaARKct has been shown to interfere with GRK2 binding to the betagamma subunits of the heterotrimeric G protein, therefore inhibiting its recruitment to the plasma membrane that normally leads to phosphorylation and internalization of the receptor. In this article we summarize the current data on the therapeutic effects of betaARKct in cardiovascular disease and report on recent and ongoing studies that may pave the way for this peptide towards therapeutic application in heart failure and other states of cardiovascular disease.
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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.