ArticleThe Journal of clinical investigation2001
Alterations in cardiac adrenergic signaling and calcium cycling differentially affect the progression of cardiomyopathy.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 187 citations in OpenAlex.
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- Canonical or non-canonical, all aspects of G protein-coupled receptor kinase 2 in heart failure.Acta physiologica (Oxford, England) · 2025Review
- Advances in pathophysiological mechanisms and therapeutic efficacy of exercise rehabilitation in patients with heart failure with preserved ejection fraction.Frontiers in cardiovascular medicine · 2025Review
- Double life: How GRK2 and β-arrestin signaling participate in diseases.Cellular signalling · 2022Review
- Shared Molecular Mechanisms of Hypertrophic Cardiomyopathy and Its Clinical Presentations: Automated Molecular Mechanisms Extraction Approach.Life (Basel, Switzerland) · 2021Article
- Guidelines for animal exercise and training protocols for cardiovascular studies.American journal of physiology. Heart and circulatory physiology · 2020Review
- Myocardial-restricted ablation of the GTPase RAD results in a pro-adaptive heart response in mice.The Journal of biological chemistry · 2019Article
- Coronary arterial vasculature in the pathophysiology of hypertrophic cardiomyopathy.Pflugers Archiv : European journal of physiology · 2019Review
- Application of G-CSF in Congestive Heart Failure Treatment.Current cardiology reviews · 2019Review
- New Insights in Cardiac β-Adrenergic Signaling During Heart Failure and Aging.Frontiers in pharmacology · 2018Review
- Promise of adeno-associated virus as a gene therapy vector for cardiovascular diseases.Heart failure reviews · 2017Review
- The expanding GRK interactome: Implications in cardiovascular disease and potential for therapeutic development.Pharmacological research · 2016Review
- Loss of Rad-GTPase produces a novel adaptive cardiac phenotype resistant to systolic decline with aging.American journal of physiology. Heart and circulatory physiology · 2015Article
- The evolving impact of g protein-coupled receptor kinases in cardiac health and disease.Physiological reviews · 2015Review
- Heart failure with preserved ejection fraction: molecular pathways of the aging myocardium.Circulation research · 2014Review
- G protein-coupled receptor kinase 2: a link between myocardial contractile function and cardiac metabolism.Circulation research · 2014Review
- The central renin-angiotensin system and sympathetic nerve activity in chronic heart failure.Clinical science (London, England : 1979) · 2014Review
- HNO enhances SERCA2a activity and cardiomyocyte function by promoting redox-dependent phospholamban oligomerization.Antioxidants & redox signaling · 2013Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
The medical treatment of chronic heart failure has undergone a dramatic transition in the past decade. Short-term approaches for altering hemodynamics have given way to long-term, reparative strategies, including beta-adrenergic receptor (betaAR) blockade. This was once viewed as counterintuitive, because acute administration causes myocardial depression. Cardiac myocytes from failing hearts show changes in betaAR signaling and excitation-contraction coupling that can impair cardiac contractility, but the role of these abnormalities in the progression of heart failure is controversial. We therefore tested the impact of different manipulations that increase contractility on the progression of cardiac dysfunction in a mouse model of hypertrophic cardiomyopathy. High-level overexpression of the beta(2)AR caused rapidly progressive cardiac failure in this model. In contrast, phospholamban ablation prevented systolic dysfunction and exercise intolerance, but not hypertrophy, in hypertrophic cardiomyopathy mice. Cardiac expression of a peptide inhibitor of the betaAR kinase 1 not only prevented systolic dysfunction and exercise intolerance but also decreased cardiac remodeling and hypertrophic gene expression. These three manipulations of cardiac contractility had distinct effects on disease progression, suggesting that selective modulation of particular aspects of betaAR signaling or excitation-contraction coupling can provide therapeutic benefit.
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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.