Reactive oxygen species-activated Ca/calmodulin kinase IIδ is required for late I(Na) augmentation leading to cellular Na and Ca overload.
about
Na⁺ transport in the normal and failing heart - remember the balanceRegulation of CaMKII signaling in cardiovascular diseaseCa(2+) signaling in the myocardium by (redox) regulation of PKA/CaMKIIThe role of late I Na in development of cardiac arrhythmiasRegulation of ion channels by pyridine nucleotidesIon Channels in the HeartAbnormal Ca(2+) cycling in failing ventricular myocytes: role of NOS1-mediated nitroso-redox balanceRegulation of intracellular Na(+) in health and disease: pathophysiological mechanisms and implications for treatmentCaMKII regulation of cardiac K channelsCaMKII-dependent regulation of cardiac Na(+) homeostasisCaMKII oxidative activation and the pathogenesis of cardiac diseaseCalmodulin-dependent protein kinase II: linking heart failure and arrhythmiasNa+ channel function, regulation, structure, trafficking and sequestrationMechanisms of ventricular arrhythmias: from molecular fluctuations to electrical turbulenceNew treatment options for late Na current, arrhythmias, and diastolic dysfunctionNew therapeutic targets in cardiology: arrhythmias and Ca2+/calmodulin-dependent kinase II (CaMKII)Mechanisms of sudden cardiac death: oxidants and metabolismTargets for therapy in sarcomeric cardiomyopathiesCalcium dysregulation in atrial fibrillation: the role of CaMKIIGeneration of highly purified human cardiomyocytes from peripheral blood mononuclear cell-derived induced pluripotent stem cellsLate Na(+) current and protracted electrical recovery are critical determinants of the aging myopathyProtein methionine oxidation augments reperfusion injury in acute ischemic strokeRole of sodium and calcium dysregulation in tachyarrhythmias in sudden cardiac death.Perspective: a dynamics-based classification of ventricular arrhythmiasPost-translational modifications of the cardiac Na channel: contribution of CaMKII-dependent phosphorylation to acquired arrhythmiasSimulation and mechanistic investigation of the arrhythmogenic role of the late sodium current in human heart failureX-ROS signalling is enhanced and graded by cyclic cardiomyocyte stretch.Ionizing radiation regulates cardiac Ca handling via increased ROS and activated CaMKII.A computational modelling approach combined with cellular electrophysiology data provides insights into the therapeutic benefit of targeting the late Na+ current.Cardiac Na Channels: Structure to FunctionA computational model predicts adjunctive pharmacotherapy for cardiac safety via selective inhibition of the late cardiac Na current.Cardiac resynchronization therapy improves altered Na channel gating in canine model of dyssynchronous heart failure.Tubulin polymerization disrupts cardiac β-adrenergic regulation of late INa.Reactive oxygen species suppress cardiac NaV1.5 expression through Foxo1.Pharmacology and Toxicology of Nav1.5-Class 1 anti-arrhythmic drugs.Intracellular Na+ overload causes oxidation of CaMKII and leads to Ca2+ mishandling in isolated ventricular myocytes.Novel aspects of excitation-contraction coupling in heart failure.Cardiac fibrosis as a determinant of ventricular tachyarrhythmias.Electrophysiologic basis for the antiarrhythmic actions of ranolazine.Xanthine oxidase inhibition alleviates the cardiac complications of insulin resistance: effect on low grade inflammation and the angiotensin system.
P2860
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P2860
Reactive oxygen species-activated Ca/calmodulin kinase IIδ is required for late I(Na) augmentation leading to cellular Na and Ca overload.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Reactive oxygen species-activated Ca/calmodulin kinase IIδ is required for late I
@nl
Reactive oxygen species-activa ...... o cellular Na and Ca overload.
@en
type
label
Reactive oxygen species-activated Ca/calmodulin kinase IIδ is required for late I
@nl
Reactive oxygen species-activa ...... o cellular Na and Ca overload.
@en
prefLabel
Reactive oxygen species-activated Ca/calmodulin kinase IIδ is required for late I
@nl
Reactive oxygen species-activa ...... o cellular Na and Ca overload.
@en
P2093
P2860
P1433
P1476
Reactive oxygen species-activa ...... to cellular Na and Ca overload
@en
P2093
Hanna M Ruff
Johannes Backs
Lars S Maier
Luiz Belardinelli
Mark E Anderson
Sarah Bellmann
Sarah L Weber
Stefan Wagner
Thomas Sowa
Timo Schulte
P2860
P304
P356
10.1161/CIRCRESAHA.110.221911
P577
2011-01-20T00:00:00Z