ArticleThe Journal of clinical investigation2003
Rescue of cardiomyocyte dysfunction by phospholamban ablation does not prevent ventricular failure in genetic hypertrophy.
Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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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
41 citing papers in PubMed, 113 citations in OpenAlex.
- Experimental Models of Hypertrophic Cardiomyopathy: A Systematic Review.JACC. Basic to translational science · 2025Review
- Protective role of triiodothyronine in sepsis‑induced cardiomyopathy through phospholamban downregulation.International journal of molecular medicine · 2025Article
- Hypertrophic cardiomyopathy inThe journal of cardiovascular aging · 2024Article
- Modifications of Sarcoplasmic Reticulum Function Prevent Progression of Sarcomere-Linked Hypertrophic Cardiomyopathy Despite a Persistent Increase in Myofilament Calcium Response.Frontiers in physiology · 2020Article
- Coronary arterial vasculature in the pathophysiology of hypertrophic cardiomyopathy.Pflugers Archiv : European journal of physiology · 2019Review
- Association of cardiac myosin-binding protein-C with the ryanodine receptor channel - putative retrograde regulation?Journal of cell science · 2018Article
- Proarrhythmic Remodeling of Calcium Homeostasis in Cardiac Disease; Implications for Diabetes and Obesity.Frontiers in physiology · 2018Review
- Palmitoyl acyltransferase Aph2 in cardiac function and the development of cardiomyopathy.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Fibroblast growth factor 21 is induced upon cardiac stress and alters cardiac lipid homeostasis.Journal of lipid research · 2014Article
- Alterations in ryanodine receptors and related proteins in heart failure.Biochimica et biophysica acta · 2013Review
- Phospholamban knockout breaks arrhythmogenic Ca²⁺ waves and suppresses catecholaminergic polymorphic ventricular tachycardia in mice.Circulation research · 2013Article
- Functional cardiac lipolysis in mice critically depends on comparative gene identification-58.The Journal of biological chemistry · 2013Article
- Novel role of HAX-1 in ischemic injury protection involvement of heat shock protein 90.Circulation research · 2013Article
- Induced overexpression of Na(+)/Ca(2+) exchanger does not aggravate myocardial dysfunction induced by transverse aortic constriction.Journal of cardiac failure · 2013Article
- Ca(2+) influx through L-type Ca(2+) channels and transient receptor potential channels activates pathological hypertrophy signaling.Journal of molecular and cellular cardiology · 2012Article
- Constitutive phosphorylation of inhibitor-1 at Ser67 and Thr75 depresses calcium cycling in cardiomyocytes and leads to remodeling upon aging.Basic research in cardiology · 2012Article
- Myosin binding protein C: implications for signal-transduction.Journal of muscle research and cell motility · 2012Review
- Long-term rescue of a familial hypertrophic cardiomyopathy caused by a mutation in the thin filament protein, tropomyosin, via modulation of a calcium cycling protein.Journal of molecular and cellular cardiology · 2011Article
- Gene therapy targets in heart failure: the path to translation.Clinical pharmacology and therapeutics · 2011Review
- Nuclear effects of G-protein receptor kinase 5 on histone deacetylase 5-regulated gene transcription in heart failure.Circulation. Heart failure · 2011Article
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
Cardiac hypertrophy, either compensated or decompensated, is associated with cardiomyocyte contractile dysfunction from depressed sarcoplasmic reticulum (SR) Ca(2+) cycling. Normalization of Ca(2+) cycling by ablation or inhibition of the SR inhibitor phospholamban (PLN) has prevented cardiac failure in experimental dilated cardiomyopathy and is a promising therapeutic approach for human heart failure. However, the potential benefits of restoring SR function on primary cardiac hypertrophy, a common antecedent of human heart failure, are unknown. We therefore tested the efficacy of PLN ablation to correct hypertrophy and contractile dysfunction in two well-characterized and highly relevant genetic mouse models of hypertrophy and cardiac failure, Galphaq overexpression and human familial hypertrophic cardiomyopathy mutant myosin binding protein C (MyBP-C(MUT)) expression. In both models, PLN ablation normalized the characteristically prolonged cardiomyocyte Ca(2+) transients and enhanced unloaded fractional shortening with no change in SR Ca(2+) pump content. However, there was no parallel improvement in in vivo cardiac function or hypertrophy in either model. Likewise, the activation of JNK and calcineurin associated with Galphaq overexpression was not affected. Thus, PLN ablation normalized contractility in isolated myocytes, but failed to rescue the cardiomyopathic phenotype elicited by activation of the Galphaq pathway or MyBP-C mutations.
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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.