Inflammatory pathways underlying atrial fibrillation

Kai Friedrichs; Anna Klinke; Stephan Baldus

doi:10.1016/j.molmed.2011.05.007

Inflammatory pathways underlying atrial fibrillation

Standard

Inflammatory pathways underlying atrial fibrillation. / Friedrichs, Kai; Klinke, Anna; Baldus, Stephan.

In: TRENDS MOL MED, Vol. 17, No. 10, 10.2011, p. 556-563.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Friedrichs, K, Klinke, A & Baldus, S 2011, 'Inflammatory pathways underlying atrial fibrillation', TRENDS MOL MED, vol. 17, no. 10, pp. 556-563. https://doi.org/10.1016/j.molmed.2011.05.007

APA

Friedrichs, K., Klinke, A., & Baldus, S. (2011). Inflammatory pathways underlying atrial fibrillation. TRENDS MOL MED, 17(10), 556-563. https://doi.org/10.1016/j.molmed.2011.05.007

Vancouver

Friedrichs K, Klinke A, Baldus S. Inflammatory pathways underlying atrial fibrillation. TRENDS MOL MED. 2011 Oct;17(10):556-563. https://doi.org/10.1016/j.molmed.2011.05.007

Bibtex

@article{c19f1d73395a482a8bcdb408b41848d3,

title = "Inflammatory pathways underlying atrial fibrillation",

abstract = "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.",

keywords = "Animals, Atrial Fibrillation/genetics, Connexins/genetics, Gene Expression Regulation, Humans, Inflammation/genetics, Leukocytes/immunology",

author = "Kai Friedrichs and Anna Klinke and Stephan Baldus",

year = "2011",

month = oct,

doi = "10.1016/j.molmed.2011.05.007",

language = "English",

volume = "17",

pages = "556--563",

journal = "TRENDS MOL MED",

issn = "1471-4914",

publisher = "Elsevier Limited",

number = "10",

}

RIS

TY - JOUR

T1 - Inflammatory pathways underlying atrial fibrillation

AU - Friedrichs, Kai

AU - Klinke, Anna

AU - Baldus, Stephan

PY - 2011/10

Y1 - 2011/10

N2 - 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.

AB - 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.

KW - Animals

KW - Atrial Fibrillation/genetics

KW - Connexins/genetics

KW - Gene Expression Regulation

KW - Humans

KW - Inflammation/genetics

KW - Leukocytes/immunology

U2 - 10.1016/j.molmed.2011.05.007

DO - 10.1016/j.molmed.2011.05.007

M3 - SCORING: Review article

C2 - 21763201

VL - 17

SP - 556

EP - 563

JO - TRENDS MOL MED

JF - TRENDS MOL MED

SN - 1471-4914

IS - 10

ER -