Ion channel dysfunction and fibrosis in atrial fibrillation: Two sides of the same coin

Author:

Arabia Gianmarco12ORCID,Bellicini Maria Giulia1,Cersosimo Angelica1,Memo Maurizio2,Mazzarotto Francesco23,Inciardi Riccardo Maria1,Cerini Manuel1ORCID,Chen Lin Yee4,Aboelhassan Mohamed5,Benzoni Patrizia6,Mitacchione Gianfranco7,Bontempi Luca8ORCID,Curnis Antonio12

Affiliation:

1. Cardiology Department Spedali Civili Hospital University of Brescia Brescia Italy

2. Department of Molecular and Translational Medicine University of Brescia Brescia Italy

3. National Heart and Lung Institute Imperial College London (F.M., J. Ware) London UK

4. University of Minnesota (L.Y.C.) Minneapolis USA

5. Cardiology Department Assiut University Heart Hospital Assiut Egypt

6. Department of Biosciences Università degli Studi di Milano Milan Italy

7. Department of Cardiology Luigi Sacco University Hospital Milan Italy

8. Unit of Cardiology, Cardiac Electrophysiology and Electrostimulation Laboratory “Bolognini” Hospital of Seriate ‐ ASST Bergamo Est Bergamo Italy

Abstract

AbstractBackgroundAtrial fibrillation (AF) is a common heart rhythm disorder that is associated with an increased risk of stroke and heart failure (HF). Initially, an association between AF and ion channel dysfunction was identified, classifying the pathology as a predominantly electrical disease. More recently it has been recognized that fibrosis and structural atrial remodeling play a driving role in the development of this arrhythmia also in these cases.PurposeUnderstanding the role of fibrosis in genetic determined AF could be important to better comprise the pathophysiology of this arrhythmia and to refine its management also in nongenetic forms. In this review we analyze genetic and epigenetic mechanisms responsible for AF and their link with atrial fibrosis, then we will consider analogies with the pathophysiological mechanism in nongenetic AF, and discuss consequent therapeutic options.

Publisher

Wiley

Cited by 1 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3