scispace - formally typeset
Open AccessJournal ArticleDOI

Recent advances in the molecular pathophysiology of atrial fibrillation

Reads0
Chats0
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.

read more

Content maybe subject to copyright    Report

Citations
More filters
Journal ArticleDOI

Biological significance of miR-126 expression in atrial fibrillation and heart failure

TL;DR: Serum miR-126 levels could serve as a potential candidate biomarker for evaluating the severity of AF and HF, but future studies with a larger and diverse patient population are necessary to confirm these results.
Journal ArticleDOI

Evidence for functional expression of TRPM7 channels in human atrial myocytes

TL;DR: It is demonstrated for the first time that functional TRPM7 channels are present in human atrial myocytes, and the channel expression is upregulated in the atria with atrial fibrillation.
Journal ArticleDOI

Calcium signalling microdomains and the t-tubular system in atrial mycoytes: potential roles in cardiac disease and arrhythmias.

TL;DR: The presence of T-tubules in the atria of large mammals may serve to accelerate changes in the amplitude of the systolic Ca(2+) transient during inotropic manoeuvres and lower diastolic [Ca(2+)](i).
Journal ArticleDOI

Overexpression of miR-27b-3p Targeting Wnt3a Regulates the Signaling Pathway of Wnt/β-Catenin and Attenuates Atrial Fibrosis in Rats with Atrial Fibrillation.

TL;DR: The results showed that miR-27b-3p overexpression could reduce the incidence and duration of AF, alleviate atrial fibrosis, increase atrial CX43 expression, and decrease the expression of Collagen-I, a-SMA,Collagen-III, TGF-β1, Wnt3a, and p-β-Catenin.
Journal ArticleDOI

Hyperuricemia and Atrial Fibrillation.

TL;DR: To investigate the link between hyperuricemia and AF, it is necessary to refer to hyperuricaemia-induced atrial remodeling, and targeting UATs might become a potential strategy to reduce the risk of hyperURicemia- induced atrial fibrillation.
References
More filters
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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.
Related Papers (5)