ArticleJournal of molecular and cellular cardiology2004
Post-transcriptional alterations in the expression of cardiac Na+ channel subunits in chronic heart failure.
Article in Journal of molecular and cellular cardiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- Cardiac radiotherapy induces electrical conduction reprogramming in the absence of transmural fibrosis.Nature communications · 2021Trial
- Resveratrol suppresses susceptibility of ventricular arrhythmia in heart failure model.BMC cardiovascular disorders · 2025Article
- MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts.iScience · 2024Article
- Article
- Preventing unfolded protein response-induced ion channel dysregulation to treat arrhythmias.Trends in molecular medicine · 2022Review
- Impact of High-Dose Irradiation on Human iPSC-Derived Cardiomyocytes Using Multi-Electrode Arrays: Implications for the Antiarrhythmic Effects of Cardiac Radioablation.International journal of molecular sciences · 2021Article
- Arrhythmogenic Remodeling in the Failing Heart.Cells · 2021Review
- Inhibition of the unfolded protein response reduces arrhythmia risk after myocardial infarction.The Journal of clinical investigation · 2021Article
- A single injection of periostin decreases cardiac voltage-gated NaThe Journal of veterinary medical science · 2021Article
- Proteomic and functional mapping of cardiac NaV1.5 channel phosphorylation sites.The Journal of general physiology · 2021Article
- The endosomal trafficking regulator LITAF controls the cardiac Nav1.5 channel via the ubiquitin ligase NEDD4-2.The Journal of biological chemistry · 2020Article
- miR-125 family regulates XIRP1 and FIH in response to myocardial infarction.Physiological genomics · 2020Article
- Genetic basis and molecular biology of cardiac arrhythmias in cardiomyopathies.Cardiovascular research · 2020Review
- Tetrodotoxin-Sensitive Neuronal-Type NaJournal of the American Heart Association · 2020Article
- The functional consequences of sodium channel NaESC heart failure · 2019Article
- Article
- Cardiac Sodium Channel Mutations: Why so Many Phenotypes?Current topics in membranes · 2016Article
- Ion Channels in the Heart.Comprehensive Physiology · 2015Review
- Contribution of sodium channel neuronal isoform Nav1.1 to late sodium current in ventricular myocytes from failing hearts.The Journal of physiology · 2015Article
- Article
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Authors and funding
5 authors.
Funding
Abstract
Clinical and experimental evidence has recently accumulated about the importance of alterations of Na(+) channel (NaCh) function and slow myocardial conduction for arrhythmias in infarcted and failing hearts (i.e., heart failure, HF). The present study evaluated the molecular mechanisms of local alterations in the expression of NaCh subunits which underlie Na(+) current (I(Na)) density decrease in HF. HF was induced in five dogs by sequential coronary microembolization and developed approximately 3 months after the last embolization (left ventricle (LV), ejection fraction = 27 +/- 7%). Five normal dogs served as a control group. Ventricular cardiomyocytes were isolated enzymatically from LV mid-myocardium and I(Na) was measured by whole-cell patch-clamp. The mRNA encoding the cardiac-specific NaCh alpha-subunit Na(v)1.5, and one of its auxiliary subunits beta 1 (NaCh beta 1), were analyzed by competitive reverse transcription-polymerase chain reaction. Protein levels of Na(v)1.5, NaCh beta 1 and NaCh beta 2 were evaluated by western blotting. The maximum density of I(Na)/C(m) was decreased in HF (n = 5) compared to control hearts (33.2 +/- 4.4 vs. 50.0 +/- 4.9 pA/pF, mean +/- S.E.M., n = 5, P < 0.05). The steady-state inactivation and activation of I(Na) remained unchanged in HF compared to control hearts. The levels of mRNA encoding Na(v)1.5, and NaCh beta 1 were unaltered in FH. However, Na(v)1.5 protein expression was reduced about 30% in HF, while NaCh beta 1 and NaCh beta 2 protein were unchanged. We conclude that experimental HF in dogs results in post-transcriptional changes in cardiac NaCh alpha-subunit expression.
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