ArticleCirculation. Cardiovascular genetics2014
Kcne2 deletion creates a multisystem syndrome predisposing to sudden cardiac death.
Article in Circulation. Cardiovascular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- KCNE gene family: From basic functions to diseases.Genes & diseases · 2026Review
- Functions of the KCNE Gene Family in Ion Channels.Biochemical genetics · 2026Review
- Review
- Canagliflozin Pretreatment Attenuates Myocardial Dysfunction and Improves Postcardiac Arrest Outcomes After Cardiac Arrest and Cardiopulmonary Resuscitation in Mice.Cardiovascular drugs and therapy · 2024Article
- Kv Channel Ancillary Subunits: Where Do We Go from Here?Physiology (Bethesda, Md.) · 2022Review
- Animal Models to Study Cardiac Arrhythmias.Circulation research · 2022Review
- The focal adhesion protein Testin modulates KCNE2 potassium channel β subunit activity.Channels (Austin, Tex.) · 2021Article
- Fluorescence Fluctuation Spectroscopy enables quantification of potassium channel subunit dynamics and stoichiometry.Scientific reports · 2021Article
- Hypochlorhydria reduces mortality in heart failure caused by Kcne2 gene deletion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The KCNE2 potassium channel β subunit is required for normal lung function and resilience to ischemia and reperfusion injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Deletion in mice of X-linked, Brugada syndrome- and atrial fibrillation-associated Kcne5 augments ventricular KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- AKT and ERK1/2 activation via remote ischemic preconditioning prevents Kcne2-dependent sudden cardiac death.Physiological reports · 2019Article
- The genetic architecture of long QT syndrome: A critical reappraisal.Trends in cardiovascular medicine · 2018Review
- Kcne4 deletion sex-specifically predisposes to cardiac arrhythmia via testosterone-dependent impairment of RISK/SAFE pathway induction in aged mice.Scientific reports · 2018Article
- Diabetes and Arrhythmias: Pathophysiology, Mechanisms and Therapeutic Outcomes.Frontiers in physiology · 2018Review
- Chansporter complexes in cell signaling.FEBS letters · 2017Review
- Involvement of glycogen synthase kinase-3β in liver ischemic conditioning induced cardioprotection against myocardial ischemia and reperfusion injury in rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
- Remote ischemic preconditioning differentially attenuates post-ischemic cardiac arrhythmia in streptozotocin-induced diabetic versus nondiabetic rats.Cardiovascular diabetology · 2017Article
- β Subunits Control the Effects of Human Kv4.3 Potassium Channel Phosphorylation.Frontiers in physiology · 2017Article
- Functional Analysis of the Coronary Heart Disease Risk Locus on Chromosome 21q22.Disease markers · 2017Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSudden cardiac death (SCD) is the leading global cause of mortality, exhibiting increased incidence in patients with diabetes mellitus. Ion channel gene perturbations provide a well-established ventricular arrhythmogenic substrate for SCD. However, most arrhythmia-susceptibility genes, including the KCNE2 K(+) channel β subunit, are expressed in multiple tissues, suggesting potential multiplex SCD substrates. METHODS AND
resultsUsing whole-transcript transcriptomics, we uncovered cardiac angiotensinogen upregulation and remodeling of cardiac angiotensinogen interaction networks in P21 Kcne2(-/-) mouse pups and adrenal remodeling consistent with metabolic syndrome in adult Kcne2(-/-) mice. This led to the discovery that Kcne2 disruption causes multiple acknowledged SCD substrates of extracardiac origin: diabetes mellitus, hypercholesterolemia, hyperkalemia, anemia, and elevated angiotensin II. Kcne2 deletion was also a prerequisite for aging-dependent QT prolongation, ventricular fibrillation and SCD immediately after transient ischemia, and fasting-dependent hypoglycemia, myocardial ischemia, and AV block.
conclusionsDisruption of a single, widely expressed arrhythmia-susceptibility gene can generate a multisystem syndrome comprising manifold electric and systemic substrates and triggers of SCD. This paradigm is expected to apply to other arrhythmia-susceptibility genes, the majority of which encode ubiquitously expressed ion channel subunits or regulatory proteins.
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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.