ArticleJournal of cardiac failure2011
β-Adrenergic receptor stimulation and activation of protein kinase A protect against α1-adrenergic-mediated phosphorylation of protein kinase D and histone deacetylase 5.
Article in Journal of cardiac failure, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- The multifactorial role of HDAC9 at the maternal-fetal interface in the pathogenesis of preeclampsia.Clinical science (London, England : 1979) · 2025Review
- Identifying Pathogenic Variants in Vietnamese Children with Functional Single Ventricle Based on Whole-Exome Sequencing.Diagnostics (Basel, Switzerland) · 2025Article
- Muscle-specific isoforms of FXR1 are necessary for miR-1-mediated repression of connexin 43 and are downregulated in pediatric dilated cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025Article
- Salbutamol attenuates arrhythmogenic effect of aminophylline in a hPSC-derived cardiac model.Scientific reports · 2024Article
- LMK235 ameliorates inflammation and fibrosis after myocardial infarction by inhibiting LSD1-related pathway.Scientific reports · 2024Article
- Article
- Serum circulating proteins from pediatric patients with dilated cardiomyopathy cause pathologic remodeling and cardiomyocyte stiffness.JCI insight · 2021Article
- Adaptive versus maladaptive cardiac remodelling in response to sustained β-adrenergic stimulation in a new 'ISO on/off model'.PloS one · 2021Article
- Heart failure in single right ventricle congenital heart disease: physiological and molecular considerations.American journal of physiology. Heart and circulatory physiology · 2020Review
- mAKAPβ signalosomes - A nodal regulator of gene transcription associated with pathological cardiac remodeling.Cellular signalling · 2019Review
- Nucleocytoplasmic export of HDAC5 and SIRT2 downregulation: two epigenetic mechanisms by which antidepressants enhance synaptic plasticity markers.Psychopharmacology · 2018Article
- Phosphodiesterase-5 Is Elevated in Failing Single Ventricle Myocardium and Affects Cardiomyocyte Remodeling In Vitro.Circulation. Heart failure · 2018Article
- Bidirectional regulation of HDAC5 by mAKAPβ signalosomes in cardiac myocytes.Journal of molecular and cellular cardiology · 2018Article
- NF2 signaling pathway plays a pro-apoptotic role in β-adrenergic receptor stimulated cardiac myocyte apoptosis.PloS one · 2018Article
- Optimization of phenol-chloroform RNA extraction.MethodsX · 2018Article
- β-Adrenergic Stimulation Induces Histone Deacetylase 5 (HDAC5) Nuclear Accumulation in Cardiomyocytes by B55α-PP2A-Mediated Dephosphorylation.Journal of the American Heart Association · 2017Article
- Emergency Spatiotemporal Shift: The Response of Protein Kinase D to Stress Signals in the Cardiovascular System.Frontiers in pharmacology · 2017Review
- Post-translational modifications regulate class IIa histone deacetylase (HDAC) function in health and disease.Molecular & cellular proteomics : MCP · 2015Review
- Regulation of CaMKII signaling in cardiovascular disease.Frontiers in pharmacology · 2015Review
- Essential role of sympathetic endothelin A receptors for adverse cardiac remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
introductionChronic activation of β(1)-adrenergic receptor (β(1)-AR) signaling can have deleterious effects on the heart, and animal models overexpressing β(1)-ARs develop a dilated cardiomyopathy and heart failure. In the classic β-AR pathway, receptor occupancy by an agonist results in increased cyclic adenosine monophosphate (cAMP) levels and activation of protein kinase A (PKA). However, the role of PKA-dependent signaling in the development and progression of cardiomyopathies and heart failure is controversial, because β-AR signal transduction is generally desensitized in the failing heart and PKA activity is not increased. METHODS AND
resultsNeonatal rat ventricular myocytes were acutely (15 minutes) or chronically (48 hours) treated with isoproterenol, and phosphorylation of protein kinase D (PKD) and histone deacetylase 5 (HDAC5) was measured. Acute β(1)-AR stimulation or expression of constitutively active (CA) PKA reduced α(1)-adrenergic-mediated phosphorylation of HDAC5 and PKD by activation of a phosphatase. Overexpression of CA-PKA also reduced α(1)-adrenergic-mediated increased expression of contractile protein fetal isoforms and promoted repression of adult isoforms, but had no effect on α(1)-adrenergic-mediated cellular hypertrophy.
conclusionsThese data indicate that the PKA-dependent arm of β-AR signaling can be antihypertrophic and presumably beneficial, through dephosphorylation of PKD and HDAC5 and reduction of hypertrophic fetal isoform gene expression.
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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.