ArticleFrontiers in physiology2012
Impact of KChIP2 on Cardiac Electrophysiology and the Progression of Heart Failure.
Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Sequencing in over 50,000 cases identifies coding and structural variation underlying atrial fibrillation risk.Nature genetics · 2025Pooled it
- Slow calcium removal contributes to impaired lusitropic response to β-adrenergic stimulation in HFpEF mice.The Journal of physiology · 2026Article
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- Increased GIRK channel activity prevents arrhythmia in mice with heart failure by enhancing ventricular repolarization.Scientific reports · 2023Article
- Systematic discovery of transcription factors that improve hPSC-derived cardiomyocyte maturation via temporal analysis of bioengineered cardiac tissues.APL bioengineering · 2023Article
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- Circadian Rhythms of Early Afterdepolarizations and Ventricular Arrhythmias in a Cardiomyocyte Model.Biophysical journal · 2021Article
- Palmitoylation: A Fatty Regulator of Myocardial Electrophysiology.Frontiers in physiology · 2020Review
- Many Cells Make Life Work-Multicellularity in Stem Cell-Based Cardiac Disease Modelling.International journal of molecular sciences · 2018Review
- Modulation of human Kv4.3/KChIP2 channel inactivation kinetics by cytoplasmic CaPflugers Archiv : European journal of physiology · 2017Article
- KChIP2 genotype dependence of transient outward current (Ito) properties in cardiomyocytes isolated from male and female mice.PloS one · 2017Article
- Cardiovascular Action of Insulin in Health and Disease: Endothelial L-Arginine Transport and Cardiac Voltage-Dependent Potassium Channels.Frontiers in physiology · 2016Review
- Kv4.3-Encoded Fast Transient Outward Current Is Presented in Kv4.2 Knockout Mouse Cardiomyocytes.PloS one · 2015Article
- Development of heart failure is independent of K+ channel-interacting protein 2 expression.The Journal of physiology · 2013Article
- Distinctive profile of IsomiR expression and novel microRNAs in rat heart left ventricle.PloS one · 2013Article
- Transgenic models of cardiac arrhythmias and sudden death.Frontiers in physiology · 2013Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Electrophysiological remodeling of cardiac potassium ion channels is important in the progression of heart failure. A reduction of the transient outward potassium current (I(to)) in mammalian heart failure is consistent with a reduced expression of potassium channel interacting protein 2 (KChIP2, a K(V)4 subunit). Approaches have been made to investigate the role of KChIP2 in shaping cardiac I(to), including the use of transgenic KChIP2 deficient mice and viral overexpression of KChIP2. The interplay between I(to) and myocardial calcium handling is pivotal in the development of heart failure, and is further strengthened by the dual role of KChIP2 as a functional subunit on both K(V)4 and Ca(V)1.2. Moreover, the potential arrhythmogenic consequence of reduced I(to) may contribute to the high relative incidence of sudden death in the early phases of human heart failure. With this review, we offer an overview of the insights into the physiological and pathological roles of KChIP2 and we discuss the limitations of translating the molecular basis of electrophysiological remodeling from animal models of heart failure to the clinical setting.
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