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Recent advances in the molecular pathophysiology of atrial fibrillation

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TLDR
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.
Abstract
Atrial fibrillation (AF) is an extremely common cardiac rhythm disorder that causes substantial morbidity and contributes to mortality. The mechanisms underlying AF are complex, involving both increased spontaneous ectopic firing of atrial cells and impulse reentry through atrial tissue. Over the past ten years, there has been enormous progress in understanding the underlying molecular pathobiology. This article reviews the basic mechanisms and molecular processes causing AF. We discuss the ways in which cardiac disease states, extracardiac factors, and abnormal genetic control lead to the arrhythmia. We conclude with a discussion of the potential therapeutic implications that might arise from an improved mechanistic understanding.

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Journal ArticleDOI

Biological therapies targeting arrhythmias: are cells and genes the answer?

TL;DR: The present review explores the cellular and genetic mechanisms leading to arrhythmias as well as the progress that has been made in using both gene and cell therapy to treat tachy- and bradyarrhythmia, and considers why this is not applicable in routine clinical practice.
Posted ContentDOI

Integrative human atrial modeling unravels interactive PKA and CaMKII signaling as key determinant of atrial arrhythmogenesis

TL;DR: A novel computational framework for simulating electrophysiology and Ca2+-handling in human atrial cardiomyocytes and tissues and their regulation by key upstream signaling pathways involved in AF-pathogenesis is built, revealing a novel synergistic crosstalk between PKA and CaMKII that promotes atrialCardiomyocyte electrical instability and arrhythmogenic triggered activity.

Function Study of Atrial Fibrillation-Linked Connexin Mutants and Heterotypic Docking Compatibility of Cardiac Connexins

Willy G Ye
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Journal ArticleDOI

Insights into Concomitant Atrial Fibrillation and Chronic Kidney Disease.

TL;DR: A review of the possible molecular mechanisms linking CKD to AF and existing therapeutic options is described to help formulate a normative therapeutic schedule for the AF population concomitant with CKD especially those with end-stage kidney failure.
References
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Journal ArticleDOI

Spontaneous Initiation of Atrial Fibrillation by Ectopic Beats Originating in the Pulmonary Veins

TL;DR: The pulmonary veins are an important source of ectopic beats, initiating frequent paroxysms of atrial fibrillation and these foci respond to treatment with radio-frequency ablation.
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Atrial Fibrillation Begets Atrial Fibrillation A Study in Awake Chronically Instrumented Goats

TL;DR: Artificial maintenance of AF leads to a marked shortening of AERP, a reversion of its physiological rate adaptation, and an increase in rate, inducibility and stability of AF.
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Secular Trends in Incidence of Atrial Fibrillation in Olmsted County, Minnesota, 1980 to 2000, and Implications on the Projections for Future Prevalence

TL;DR: The age-adjusted incidence of AF increased significantly in Olmsted County during 1980 to 2000 and the projected number of persons with AF for the United States will exceed 10 million by 2050, underscoring the urgent need for primary prevention strategies against AF development.
Journal ArticleDOI

Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis

TL;DR: It is concluded that miR-29 acts as a regulator of cardiac fibrosis and represents a potential therapeutic target for tissue fibrosis in general.
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