Affiliation:
1. From the Mayo Clinic Windland Smith Rice Sudden Death Genomics Laboratory (M.J.A.); and Departments of Medicine, Pediatrics, and Molecular Pharmacology & Experimental Therapeutics/Divisions of Cardiovascular Diseases and Pediatric Cardiology (M.J.A.), Mayo Clinic, Rochester, Minn; and Department of Internal Medicine, Division of Cardiovascular Medicine (P.J.M.); and Department of Molecular Physiology & Biophysics (P.J.M.), University of Iowa Carver College of Medicine, Iowa City.
Abstract
Abstract:
Over the past 15 years, gene mutations in cardiac ion channels have been linked to a host of potentially fatal human arrhythmias including long QT syndrome, short QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia. More recently, a new paradigm for human arrhythmia has emerged based on gene mutations that affect the activity of cardiac ion channel- and transporter- associated proteins. As part of the
Circulation Research
thematic series on inherited arrhythmias, this review focuses on the emerging field of human arrhythmias caused by dysfunction in cytosolic gene products (including ankyrins, yotiao, syntrophin, and caveolin-3) that regulate the activities of key membrane ion channels and transporters.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine,Physiology
Cited by
64 articles.
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