ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Rescue of Ca2+ overload-induced left ventricular dysfunction by targeted ablation of phospholamban.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 44 citations in OpenAlex.
- Allosteric Modulation of SERCA Pumps in Health and Disease: Structural Dynamics, Posttranslational Modifications, and Therapeutic Potential.Journal of molecular biology · 2025Review
- Intratracheal Delivery of a Phospholamban Decoy Peptide Attenuates Cardiac Damage Following Myocardial Infarction.International journal of molecular sciences · 2025Article
- Multiscale computational modeling of the effects of 2'-deoxy-ATP on cardiac muscle calcium handling.Journal of applied physics · 2023Article
- Phospholamban pentamerization increases sensitivity and dynamic range of cardiac relaxation.Cardiovascular research · 2023Article
- Understanding the Role of SERCA2a Microdomain Remodeling in Heart Failure Induced by Obesity and Type 2 Diabetes.Journal of cardiovascular development and disease · 2022Review
- The Effects of Neuropeptide Y Overexpression on the Mouse Model of Doxorubicin-Induced Cardiotoxicity.Cardiovascular toxicology · 2020Article
- Calcium Mechanisms in Limb-Girdle Muscular Dystrophy withInternational journal of molecular sciences · 2019Review
- When signalling goes wrong: pathogenic variants in structural and signalling proteins causing cardiomyopathies.Journal of muscle research and cell motility · 2017Review
- Cinaciguat prevents the development of pathologic hypertrophy in a rat model of left ventricular pressure overload.Scientific reports · 2016Article
- Phospholamban phosphorylation, mutation, and structural dynamics: a biophysical approach to understanding and treating cardiomyopathy.Biophysical reviews · 2015Article
- Cardiovascular gene therapy for myocardial infarction.Expert opinion on biological therapy · 2014Review
- Myocardial gene transfer: routes and devices for regulation of transgene expression by modulation of cellular permeability.Human gene therapy · 2013Review
- Rodent models of heart failure: an updated review.Heart failure reviews · 2013Review
- Model-specific selection of molecular targets for heart failure gene therapy.The journal of gene medicine · 2011Review
- Ablation of phospholamban and sarcolipin results in cardiac hypertrophy and decreased cardiac contractility.Cardiovascular research · 2011Article
- Article
- Superoxide scavenging and Akt inhibition in myocardium ameliorate pressure overload-induced NF-κB activation and cardiac hypertrophy.Physiological genomics · 2010Article
- Sarcoplasmic reticulum Ca(2+) ATPase as a therapeutic target for heart failure.Expert opinion on biological therapy · 2010Review
- Ion channels, transporters, and pumps as targets for heart failure therapy.Journal of cardiovascular pharmacology · 2009Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
In failing hearts, a deficiency in sarco(endo)plasmic reticulum Ca2+ -ATPase (SERCA)2a results in abnormal Ca2+ handling and diminished contraction. In addition, a decrease in the phosphorylation of phospholamban (PLB) has been reported. Gene transfer of antisense PLB (asPLB) can improve contractile function in the failing human myocardium. Gene transfer of SERCA2a improves survival and the energy potential in failing hearts. The aim of present study was to evaluate whether enhancement of SERCA2a function prevents acute Ca2+ overload-induced left ventricular (LV) dysfunction in rat hearts. We ablated PLB using adenoviral gene transfer of asPLB by a new and less invasive gene delivery method, which involved a percutaneous technique. Experiments were performed on 13 excised cross-circulated rat hearts: 5 rats underwent sham operations, 4 rats underwent gene transfer of the reporter gene beta-galactosidase (Ad.beta-gal), and 4 rats underwent gene transfer of asPLB (Ad.asPLB). After clearance of high Ca2+ infused into the coronary, there was LV contractile dysfunction associated with the decreased myocardial O2 consumption per beat (Vo2) intercept (equal to decreased Vo2 for Ca2+ handling in excitation-contraction coupling) of the Vo2-systolic pressure-volume area (PVA; total mechanical energy per beat) linear relation in the hearts that underwent sham operation and had been infected with Ad.beta-gal. Hearts that had been infected with Ad.asPLB were rescued from LV contractile dysfunction associated with an unchanged Vo2 intercept of the Vo2-PVA linear relation. We conclude that SERCA2a function enhanced by adenoviral gene transfer of asPLB prevents Ca2+ overload-induced LV contractile dysfunction in terms of mechanical work and especially energetics.
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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.