ArticleJournal of cardiovascular pharmacology2018
Human Myocardium Has a Robust α1A-Subtype Adrenergic Receptor Inotropic Response.
Article in Journal of cardiovascular pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Cardiac and Vascular αCells · 2020Pooled it
- Cardiac myosin binding protein-C phosphorylation as a function of multiple protein kinase and phosphatase activities.Nature communications · 2024Article
- Increased length-dependent activation of human engineered heart tissue after chronic αAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- αInternational journal of molecular sciences · 2023Review
- Mechanisms for the α-Adrenoceptor-Mediated Positive Inotropy in Mouse Ventricular Myocardium: Enhancing Effect of Action Potential Prolongation.International journal of molecular sciences · 2023Article
- Electroacupuncture Ameliorates Acute Myocardial Ischemic Injury and Long QT Interval in Mice through theOxidative medicine and cellular longevity · 2022Article
- The Case for, and Challenges of, Human Cardiac Tissue in Advancing Phosphoprotein Research.Frontiers in physiology · 2022Review
- Sympatho-adrenergic mechanisms in heart failure: new insights into pathophysiology.Medical review (2021) · 2021Article
- α1-Adrenergic receptor regulates papillary muscle and aortic segment contractile function via modulation of store-operated CaJournal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2021Article
- Review
- Targeting Adrenergic Receptors in Metabolic Therapies for Heart Failure.International journal of molecular sciences · 2021Review
- Cardiac α1A-adrenergic receptors: emerging protective roles in cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2021Review
- Current Developments on the Role of αFrontiers in cell and developmental biology · 2021Review
- Multiparametric Mechanistic Profiling of Inotropic Drugs in Adult Human Primary Cardiomyocytes.Scientific reports · 2020Article
- Stretching single titin molecules from failing human hearts reveals titin's role in blunting cardiac kinetic reserve.Cardiovascular research · 2020Article
- Site-specific phosphorylation of myosin binding protein-C coordinates thin and thick filament activation in cardiac muscle.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Modeling heart failure in animal models for novel drug discovery and development.Expert opinion on drug discovery · 2019Review
- Reversal of right ventricular failure by chronic αAmerican journal of physiology. Heart and circulatory physiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Recent studies report that a single subtype of α1-adrenergic receptor (α1-AR), the α1A-subtype, mediates robust cardioprotective effects in multiple experimental models of heart failure, suggesting that the α1A-subtype is a potential therapeutic target for an agonist to treat heart failure. Moreover, we recently found that the α1A-subtype is present in human heart. The goal of this study was to assess the inotropic response mediated by the α1A-subtype in human myocardium, and to determine whether the response is downregulated in myocardium from failing human heart. We measured in vitro contractile responses of cardiac muscle preparations (trabeculae) isolated from the right ventricle from nonfailing and failing human hearts. Addition of the α1A-subtype agonist A61603 (100 nM) resulted in a large positive inotropic response (force increased ≈ 2-fold). This response represented ≈70% of the response mediated by the β-adrenergic receptor agonist isoproterenol (1 μM). Moreover, in myocardium from failing hearts, α1A-subtype responses remained robust, and only slightly reduced relative to nonfailing hearts. We conclude that α1A-subtype-mediated inotropy could represent a significant source of inotropic support in the human heart. Furthermore, the α1A-subtype remains functional in myocardium from failing human hearts and thus, might be a therapeutic target to support cardioprotective effects in patients with heart failure.
Indexed as
Identifiers
What OpenQuestion holds
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.