ReviewChannels (Austin, Tex.)2014
The potential role of Kv4.3 K+ channel in heart hypertrophy.
Review in Channels (Austin, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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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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
15 citing papers in PubMed, 25 citations in OpenAlex.
- Annexin A4 Deficient Ventricular Myocytes Display Advanced Hypertrophy and Electrical Remodeling With Chronic β-Adrenoceptor Stimulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Mitochondrial DNA-driven intercellular communication networks in post-infarction ventricular remodeling: the three-threshold model of cGAS-STING activation.Frontiers in immunology · 2026Review
- Mechanistic Relevance of Ventricular Arrhythmias in Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
- The Kv4 potassium channel modulator NS5806 attenuates cardiac hypertrophy in vivo and in vitro.Scientific reports · 2024Article
- Effects of JZTX-V on the wild type Kv4.3 Expressed in HEK293T and Molecular Determinants in the Voltage-sensing Domains of Kv4.3 Interacting with JZTX-V.Channels (Austin, Tex.) · 2022Article
- Modulation of KInternational journal of molecular sciences · 2022Article
- SUMOylation of the Kv4.2 Ternary Complex Increases Surface Expression and Current Amplitude by Reducing Internalization in HEK 293 Cells.Frontiers in molecular neuroscience · 2021Article
- Up-regulation of miR-195 contributes to cardiac hypertrophy-induced arrhythmia by targeting calcium and potassium channels.Journal of cellular and molecular medicine · 2020Article
- Investigation of gene-gene interactions in cardiac traits and serum fatty acid levels in the LURIC Health Study.PloS one · 2020Article
- Phase 1 repolarization rate defines CaThe Journal of general physiology · 2019Article
- Identification of IQM-266, a Novel DREAM Ligand That Modulates KFrontiers in molecular neuroscience · 2019Article
- miR-133: A Suppressor of Cardiac Remodeling?Frontiers in pharmacology · 2018Review
- Effects of allitridum on the transient outward potassium current in rats with heart failure.Journal of geriatric cardiology : JGC · 2016Article
- Zebrafish heart as a model for human cardiac electrophysiology.Channels (Austin, Tex.) · 2016Review
- Neuronal nitric oxide synthase in hypertension - an update.Clinical hypertension · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transient outward K+ current (I(to)) plays a crucial role in the early phase of cardiac action potential repolarization. Kv4.3 K(+) channel is an important component of I(to). The function and expression of Kv4.3 K(+) channel decrease in variety of heart diseases, especially in heart hypertrophy/heart failure. Int his review, we summarized the changes of cardiac Kv4.3 K(+) channel in heart diseases and discussed the potential role of Kv4.3 K(+) channel in heart hypertrophy/heart failure. In heart hypertrophy/heart failure of mice and rats, down regulation of Kv4.3 K(+) channel leads to prolongation of action potential duration (APD), which is associated with increased [Ca(2+)](I), activation of calcineurin and heart hypertrophy/heart failure.However, in canine and human, Kv4.3 K(+) channel does not play a major role in setting cardiac APD. So, in addition to Kv4.3 K(+) channel/APD/[Ca(2+)](I) pathway, there exits another mechanism of Kv4.3 K(+) channel in heart hypertrophy and heart failure: downregulation of Kv4.3 K(+) channels leads to CaMKII dissociation from Kv4.3–CaMKII complex and subsequent activation of the dissociated CaMKII , which induces heart hypertrophy/heart failure. Upregulation of Kv4.3K(+) channel inhibits CaMKII activation and its related harmful consequences. We put forward a new point-of-view that Kv4.3 K(+) channel is involved in heart hypertrophy/heart failure independently of its electric function, and drugs inhibiting or upregulating Kv4.3 K(+) channel might be potentially harmful or beneficial to hearts through CaMKII.
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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.