ArticleHeart rhythm2015
Electrophysiologic consequences of KATP gain of function in the heart: Conduction abnormalities in Cantu syndrome.
Article in Heart rhythm, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- A Unique High-Output Cardiac Hypertrophy Phenotype Arising From Low Systemic Vascular Resistance in Cantu Syndrome.Journal of the American Heart Association · 2022Article
- Case Report: Loss-of-FunctionFrontiers in genetics · 2022Article
- Cantú syndrome: Findings from 74 patients in the International Cantú Syndrome Registry.American journal of medical genetics. Part C, Seminars in medical genetics · 2019Article
- Genetic Discovery of ATP-Sensitive KCirculation. Arrhythmia and electrophysiology · 2019Review
- Ectopic overexpression of Kir6.1 in the mouse heart impacts on the life expectancy.Scientific reports · 2018Article
- ATP-sensitive potassium channels in the sinoatrial node contribute to heart rate control and adaptation to hypoxia.The Journal of biological chemistry · 2018Article
- Cantu syndrome-associated SUR2 (ABCC9) mutations in distinct structural domains result in KThe Journal of biological chemistry · 2018Article
- MiR-20 regulates myocardiac ischemia by targeting KATP subunit Kir6.1.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017Article
- Potassium channels in the heart: structure, function and regulation.The Journal of physiology · 2017Review
- Increased tolerance to stress in cardiac expressed gain-of-function of adenosine triphosphate-sensitive potassium channel subunit Kir6.1.The Journal of surgical research · 2016Article
- K(ATP) channel gain-of-function leads to increased myocardial L-type Ca(2+) current and contractility in Cantu syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Adenosine Triphosphate-Sensitive Potassium Currents in Heart Disease and Cardioprotection.Cardiac electrophysiology clinics · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundGain-of-function (GOF) mutations in the KATP channel subunits Kir6.1 and SUR2 cause Cantu syndrome (CS), a disease characterized by multiple cardiovascular abnormalities.
objectiveThe purpose of this study was to better determine the electrophysiologic consequences of such GOF mutations in the heart.
methodsWe generated transgenic mice (Kir6.1-GOF) expressing ATP-insensitive Kir6.1[G343D] subunits under α-myosin heavy chain (α-MHC) promoter control, to target gene expression specifically in cardiomyocytes, and performed patch-clamp experiments on isolated ventricular myocytes and invasive electrophysiology on anesthetized mice.
resultsIn Kir6.1-GOF ventricular myocytes, KATP channels showed decreased ATP sensitivity but no significant change in current density. Ambulatory ECG recordings on Kir6.1-GOF mice revealed AV nodal conduction abnormalities and junctional rhythm. Invasive electrophysiologic analyses revealed slowing of conduction and conduction failure through the AV node but no increase in susceptibility to atrial or ventricular ectopic activity. Surface ECGs recorded from CS patients also demonstrated first-degree AV block and fascicular block.
conclusionThe primary electrophysiologic consequence of cardiac KATP GOF is on the conduction system, particularly the AV node, resulting in conduction abnormalities in CS patients who carry KATP GOF mutations.
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