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Niels Voigt

Researcher at University of Göttingen

Publications -  131
Citations -  7369

Niels Voigt is an academic researcher from University of Göttingen. The author has contributed to research in topics: Atrial fibrillation & Ryanodine receptor. The author has an hindex of 37, co-authored 117 publications receiving 6219 citations. Previous affiliations of Niels Voigt include University of Duisburg-Essen & Dresden University of Technology.

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Enhanced Sarcoplasmic Reticulum Ca2+ Leak and Increased Na+-Ca2+ Exchanger Function Underlie Delayed Afterdepolarizations in Patients With Chronic Atrial Fibrillation

TL;DR: Enhanced SR Ca2+ leak through CaMKII-hyperphosphorylated RyR2, in combination with larger INCX for a given SR Ca 2+ release and increased diastolic [Ca2+]i-voltage coupling gain, causes AF-promoting atrial delayed afterdepolarizations/triggered activity in cAF patients.
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Recent advances in the molecular pathophysiology of atrial fibrillation

TL;DR: The ways in which cardiac disease states, extracardiac factors, and abnormal genetic control lead to the arrhythmia are discussed, including the potential therapeutic implications that might arise from an improved mechanistic understanding.
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Cellular and Molecular Electrophysiology of Atrial Fibrillation Initiation, Maintenance, and Progression

TL;DR: A comprehensive understanding of AF pathophysiology is expected to foster the development of improved pharmacological and nonpharmacological therapeutic approaches and to greatly improve clinical management.
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The G protein-gated potassium current I(K,ACh) is constitutively active in patients with chronic atrial fibrillation.

TL;DR: It is demonstrated that larger basal inward rectifier K+ current in cAF consists of increased IK1 activity and constitutively active IK,ACh, which may represent a new therapeutic target in AF.
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Cellular and Molecular Mechanisms of Atrial Arrhythmogenesis in Patients With Paroxysmal Atrial Fibrillation

TL;DR: Biochemical, functional, and modeling studies point to a combination of increased sarcoplasmic reticulum Ca2+ load related to phospholamban hyperphosphorylation and ryanodine receptor dysregulation and enhanced SERCA2a activity as underlying mechanisms for cellular arrhythmogenesis in pAF patients.