Metabolic stress, reactive oxygen species, and arrhythmia

Article ID	Journal	Published Year	Pages	File Type
10953883	Journal of Molecular and Cellular Cardiology	2012	10 Pages	PDF

Abstract

âº Cardiomyopathies are associated with metabolic stress, oxidative stress, and arrhythmic risk. âº Oxidative stress alters ion channels, Ca2+ handling, and gap junctions, possibly explaining the arrhythmic risk. âº Anti-oxidants may be useful anti-arrhythmic drugs. âº ROS mediate arrhythmogenesis through the alteration of ion homeostasis and structural remodeling.

Keywords

ADP Torsades de pointes TDP IKr mitoKATP NCX connexins ANGII RyR Nav1.5 HERG IKS NOS RAS IMAC ACE GSH SCD DTT SCN5A PES ∆ψm Mitochondrial ATP-sensitive potassium channel TCA Sarcoplasmic reticulum Ca2+-ATPase INa Na+–Ca2+ exchanger ROS [Ca2+]i adenosine-5′-triphosphate ATP adenosine diphosphate Arrhythmia angiotensin converting enzyme Angiotensin II E-C coupling tricarboxylic acid Ventricular tachycardia Programmed electrical stimulation Excitation–contraction coupling sodium current Ca2+ handling dithiothreitol Sarcoplasmic reticulum electron transport chain renin-angiotensin system intracellular Ca2+ concentration Atrial fibrillation SERCA cardiac sodium channel Sudden cardiac death Mitochondria NAD heart failure map Nitric oxide nitric oxide synthase nicotinamide adenine dinucleotide ETc action potential Mitochondrial membrane potential Monophasic action potential Protein kinase human ether-à-go-go-related gene Inner membrane anion channel Sodium Channel CICR connexin Glutathione Reactive oxygen species Ryanodine receptor