Inflammatory pathways underlying atrial fibrillation

被引：157

作者：

Friedrichs, Kai ^{[3
]}

Klinke, Anna ^{[1
,2
]}

Baldus, Stephan ^{[1
,2
]}

机构：

[1] Univ Heart Ctr Hamburg, Cardiovasc Res Ctr, D-20246 Hamburg, Germany

[2] Univ Heart Ctr Hamburg, Dept Gen & Intervent Cardiol, D-20246 Hamburg, Germany

[3] Univ Heart Ctr Hamburg, Dept Electrophysiol, D-20246 Hamburg, Germany

来源：

TRENDS IN MOLECULAR MEDICINE | 2011年 / 17卷 / 10期

关键词：

C-REACTIVE PROTEIN; PULMONARY VEIN ISOLATION; NECROSIS-FACTOR-ALPHA; NF-KAPPA-B; OXIDATIVE STRESS; CARDIAC-SURGERY; STERILE PERICARDITIS; REDOX REGULATION; TRANSGENIC MICE; NADPH OXIDASE;

D O I：

10.1016/j.molmed.2011.05.007

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The pathophysiology of atrial fibrillation (AF) remains incompletely understood, despite its prevalence and contributing role in stroke and heart failure. Whereas previous studies have focused on the electrophysiological characteristics of AF, recent reports shed light on structural remodeling of the atria as a prerequisite for AF. Recent evidence suggests that atrial fibrosis is linked not only to stimulation of myocytes and fibroblasts, but also to the activation state of leukocytes. Recruitment of leukocytes with the release of reactive oxygen species, cytokines and growth factors is followed by increased matrix deposition, which leads to adverse atrial remodeling and suggests that inflammatory pathways are a prerequisite for AF. Here we review current evidence demonstrating the interrelation between inflammation and AF.

引用

页码：556 / 563

页数：8

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