ArticleBasic research in cardiology2015
Expression and function of Kv1.1 potassium channels in human atria from patients with atrial fibrillation.
Article in Basic research in cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Sex-specific differences in mortality and neurocardiac interactions in the Kv1.1 knockout mouse model of sudden unexpected death in epilepsy (SUDEP).The Journal of physiology · 2026Article
- Cardiac-specific Kv1.1 deficiency alters cardiomyocyte electrophysiology without modifying overall cardiac function or arrhythmia susceptibility.Experimental physiology · 2026Article
- Epilepsy-associated Kv1.1 channel subunits regulate intrinsic cardiac pacemaking in mice.The Journal of general physiology · 2024Article
- The causal relationship between obesity, obstructive sleep apnea and atrial fibrillation: a study based on mediated Mendelian randomization.Frontiers in cardiovascular medicine · 2024Article
- PPP1R12C Promotes Atrial Hypocontractility in Atrial Fibrillation.Circulation research · 2023Article
- New drug discovery of cardiac anti-arrhythmic drugs: insights in animal models.Scientific reports · 2023Article
- Gene mutations in comorbidity of epilepsy and arrhythmia.Journal of neurology · 2023Review
- Animal Models to Study Cardiac Arrhythmias.Circulation research · 2022Review
- The brain-heart interaction in epilepsy: implications for diagnosis, therapy, and SUDEP prevention.Annals of clinical and translational neurology · 2021Review
- Kv1.1 potassium channel subunit deficiency alters ventricular arrhythmia susceptibility, contractility, and repolarization.Physiological reports · 2021Article
- Kv1.1 Channelopathies: Pathophysiological Mechanisms and Therapeutic Approaches.International journal of molecular sciences · 2020Review
- Clinical Spectrum ofInternational journal of molecular sciences · 2020Review
- Neuron-specific Kv1.1 deficiency is sufficient to cause epilepsy, premature death, and cardiorespiratory dysregulation.Neurobiology of disease · 2020Article
- Kv1.1 channel subunits in the control of neurocardiac function.Channels (Austin, Tex.) · 2019Review
- Cardiorespiratory profiling reveals primary breathing dysfunction in Kcna1-null mice: Implications for sudden unexpected death in epilepsy.Neurobiology of disease · 2019Article
- Genetic ablation or pharmacological inhibition of Kv1.1 potassium channel subunits impairs atrial repolarization in mice.American journal of physiology. Cell physiology · 2019Article
- Voltage-gated and stretch-activated potassium channels in the human heart : Pathophysiological and clinical significance.Herzschrittmachertherapie & Elektrophysiologie · 2018Review
- Age-Related Differential Structural and Transcriptomic Responses in the Hypertensive Heart.Frontiers in physiology · 2018Article
- Regulation of human cardiac potassium channels by full-length KCNE3 and KCNE4.Scientific reports · 2016Article
- Review
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Voltage-gated Kv1.1 channels encoded by the Kcna1 gene are traditionally regarded as being neural-specific with no known expression or intrinsic functional role in the heart. However, recent studies in mice reveal low-level Kv1.1 expression in heart and cardiac abnormalities associated with Kv1.1-deficiency suggesting that the channel may have a previously unrecognized cardiac role. Therefore, this study tests the hypothesis that Kv1.1 channels are associated with arrhythmogenesis and contribute to intrinsic cardiac function. In intra-atrial burst pacing experiments, Kcna1-null mice exhibited increased susceptibility to atrial fibrillation (AF). The atria of Kcna1-null mice showed minimal Kv1 family ion channel remodeling and fibrosis as measured by qRT-PCR and Masson's trichrome histology, respectively. Using RT-PCR, immunocytochemistry, and immunoblotting, KCNA1 mRNA and protein were detected in isolated mouse cardiomyocytes and human atria for the first time. Patients with chronic AF (cAF) showed no changes in KCNA1 mRNA levels relative to controls; however, they exhibited increases in atrial Kv1.1 protein levels, not seen in paroxysmal AF patients. Patch-clamp recordings of isolated human atrial myocytes revealed significant dendrotoxin-K (DTX-K)-sensitive outward current components that were significantly increased in cAF patients, reflecting a contribution by Kv1.1 channels. The concomitant increases in Kv1.1 protein and DTX-K-sensitive currents in atria of cAF patients suggest that the channel contributes to the pathological mechanisms of persistent AF. These findings provide evidence of an intrinsic cardiac role of Kv1.1 channels and indicate that they may contribute to atrial repolarization and AF susceptibility.
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