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Review
. 2019 Jul 15:287:195-200.
doi: 10.1016/j.ijcard.2018.10.020. Epub 2018 Oct 4.

Role of inflammatory signaling in atrial fibrillation

Larry Scott Jr  1 , Na Li  2 , Dobromir Dobrev  3
Affiliations
Review

Role of inflammatory signaling in atrial fibrillation

Larry Scott Jr et al. Int J Cardiol. .

Abstract

Atrial fibrillation (AF), the most prevalent arrhythmia, is often associated with enhanced inflammatory response. Emerging evidence points to a causal role of inflammatory signaling pathways in the evolution of atrial electrical, calcium handling and structural remodeling, which create the substrate of AF development. In this review, we discuss the clinical evidence supporting the association between inflammatory indices and AF development, the molecular and cellular mechanisms of AF, which appear to involve multiple canonical inflammatory pathways, and the potential of anti-inflammatory therapeutic approaches in AF prevention/treatment.

Keywords: Atrial fibrillation; IL-1β; Inflammasome; Inflammation; NFκB; TNF-α.

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Figures

Figure 1.
Figure 1.. Fundamental mechanisms of atrial fibrillation (AF) and potential contribution of inflammation and inflammatory signaling to the evolution of AF-promoting ectopic activity and reentry.
ANS, autonomic nervous system; APD, action potential duration; EADs, early afterdepolorizations; ERP, effective refractory period; DADs, delayed afterdepolorizations.
Figure 2.
Figure 2.. Putative molecular and cellular mechanisms of atrial fibrillation pathogenesis involving inflammatory pathways.
APD, action potential duration; ATP, adenosine triphosphate; EADs, early afterdepolorizations; ECM, extracellular matrix; ERP, effective refractory period; DADs, delayed afterdepolorizations; DAMPs, damage-associated molecular patterns; JNK, c-Jun N-terminal kinase; MAPK, activated protein kinase mitogen; P2X7R, P2X purinoceptor 7; SR, sarcoplasmic reticulum.
Figure 3
Figure 3. Proposed therapeutic strategies for AF by targeting inflammatory pathways.
. APD, action potential duration; ATP, adenosine triphosphate; EADs, early afterdepolorizations; ECM, extracellular matrix; ERP, effective refractory period; DADs, delayed afterdepolorizations; DAMPs, damage-associated molecular patterns; JNK, c-Jun N-terminal kinase; MAPK, activated protein kinase mitogen; P2X7R, P2X purinoceptor 7; SR, sarcoplasmic reticulum.
See this image and copyright information in PMC

References

    1. Feigin VL, Norrving B, Mensah GA. Global Burden of Stroke. Circ Res. 120 (2017) 439–448. - PubMed
    1. Iwasaki YK, Nishida K, Kato T, Nattel S. Atrial fibrillation pathophysiology: implications for management. Circulation. 124 (2011) 2264–2274. - PubMed
    1. Schnabel RB, Yin X, Gona P, Larson MG, Beiser AS, McManus DD, et al. 50 year trends in atrial fibrillation prevalence, incidence, risk factors, and mortality in the Framingham Heart Study: a cohort study. Lancet (London, England). 386 (2015) 154–162. - PMC - PubMed
    1. Andrade J, Khairy P, Dobrev D, Nattel S. The clinical profile and pathophysiology of atrial fibrillation: relationships among clinical features, epidemiology, and mechanisms. Circ Res. 114, (2014) 1453–1468. - PubMed
    1. Gheorghe-Andrei D, Dobrev D Antiarrhythmic drugs for atrial fibrillation: Imminent impulses are emerging. IJC Heart & Vasculature. 21 (2018) 11–15. - PMC - PubMed

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