Multiple potential molecular contributors to atrial hypocontractility caused by atrial tachycardia remodeling in dogs. - Wikidata - wikimedia - TriplyDB

Multiple potential molecular contributors to atrial hypocontractility caused by atrial tachycardia remodeling in dogs.

Multiple potential molecular contributors to atrial hypocontractility caused by atrial tachycardia remodeling in dogs.

http://www.wikidata.org/entity/Q34128043

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Calcium dysregulation in atrial fibrillation: the role of CaMKII In silico screening of the key cellular remodeling targets in chronic atrial fibrillation Association between left atrial low-voltage area, serum apoptosis, and fibrosis biomarkers and incidence of silent cerebral events after catheter ablation of atrial fibrillation.Regulation of Cardiomyocyte T-Tubular Structure: Opportunities for Therapy.Ca(2+) homeostasis in sealed t-tubules of mouse ventricular myocytes.SR calcium handling dysfunction, stress-response signaling pathways, and atrial fibrillation.Cellular and molecular mechanisms of atrial arrhythmogenesis in patients with paroxysmal atrial fibrillation.Tachycardia-induced silencing of subcellular Ca2+ signaling in atrial myocytes.Atrial fibrillation complicated by heart failure induces distinct remodeling of calcium cycling proteins Transverse tubules are a common feature in large mammalian atrial myocytes including human.Enhanced sarcoplasmic reticulum Ca2+ leak and increased Na+-Ca2+ exchanger function underlie delayed afterdepolarizations in patients with chronic atrial fibrillation.Electro-mechanical dynamics of spiral waves in a discrete 2D model of human atrial tissue Direct Evidence for Microdomain-Specific Localization and Remodeling of Functional L-Type Calcium Channels in Rat and Human Atrial Myocytes.Atrial remodelling in atrial fibrillation: CaMKII as a nodal proarrhythmic signal Chronic myocardial infarction promotes atrial action potential alternans, afterdepolarizations, and fibrillation.Altered Excitation-Contraction Coupling in Human Chronic Atrial Fibrillation.Atrial fibrillation: mechanisms, therapeutics, and future directions.The ryanodine receptor channel as a molecular motif in atrial fibrillation: pathophysiological and therapeutic implications.Novel molecular targets for atrial fibrillation therapy.New directions in antiarrhythmic drug therapy for atrial fibrillation.The transverse-axial tubular system of cardiomyocytes.Serine/Threonine Phosphatases in Atrial Fibrillation.Current controversies in determining the main mechanisms of atrial fibrillation.The Stress-Response MAP Kinase Signaling in Cardiac Arrhythmias.Anti-arrhythmic strategies for atrial fibrillation: The role of computational modeling in discovery, development, and optimization.Regulating the regulator: Insights into the cardiac protein phosphatase 1 interactome.Transforming growth factor-β and oxidative stress mediate tachycardia-induced cellular remodelling in cultured atrial-derived myocytes.[AFNET. A translational research network develops into an academic research organization].Persistence of pro-arrhythmic spatio-temporal calcium patterns in atrial myocytes: a computational study of ping waves.Calcium signalling microdomains and the t-tubular system in atrial mycoytes: potential roles in cardiac disease and arrhythmias.Heterogeneity of transverse-axial tubule system in mouse atria: Remodeling in atrial-specific Na+-Ca2+ exchanger knockout mice.Calcium signalling silencing in atrial fibrillation.Response to exercise and mechanical efficiency in non-ischaemic stunning, induced by short-term rapid pacing in dogs: a role for calcium?Age-dependent Increase in JNK2 Activity: Does This Help to Understand CaMKII-mediated Atrial Arrhythmogenesis in Human Atrial Fibrillation?Variable t-tubule organization and Ca2+ homeostasis across the atria.Cellular and molecular correlates of ectopic activity in patients with atrial fibrillation.Cathepsin A mediates susceptibility to atrial tachyarrhythmia and impairment of atrial emptying function in Zucker diabetic fatty rats.Ca2+/Calmodulin-Dependent Protein Kinase II (CaMKII) Increases Small-Conductance Ca2+-Activated K+ Current in Patients with Chronic Atrial Fibrillation.Computational Modeling of Electrophysiology and Pharmacotherapy of Atrial Fibrillation: Recent Advances and Future Challenges Axial Tubule Junctions Activate Atrial Ca Release Across Species

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P2860

Multiple potential molecular contributors to atrial hypocontractility caused by atrial tachycardia remodeling in dogs.

http://www.wikidata.org/entity/Q34128043

description

2010 nî lūn-bûn

@nan

2010 թուականի Յուլիսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հուլիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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Multiple potential molecular c ...... achycardia remodeling in dogs.

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Multiple potential molecular c ...... achycardia remodeling in dogs.

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Multiple potential molecular c ...... achycardia remodeling in dogs.

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type

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Multiple potential molecular c ...... achycardia remodeling in dogs.

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Multiple potential molecular c ...... achycardia remodeling in dogs.

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Multiple potential molecular c ...... achycardia remodeling in dogs.

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Multiple potential molecular c ...... achycardia remodeling in dogs.

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Multiple potential molecular c ...... achycardia remodeling in dogs.

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Multiple potential molecular c ...... achycardia remodeling in dogs.

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Multiple potential molecular c ...... tachycardia remodeling in dogs

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Ange Maguy

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Denis Chartier

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Dobromir Dobrev

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Jean-Claude Tardif

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Kunihiro Nishida

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Louis-Robert Villeneuve

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