Human epicardial adipose tissue induces fibrosis of the atrial myocardium through the secretion of adipo-fibrokines

Venteclef, Nicolas; Guglielmi, Valeria; Balse, Elise; Gaborit, Bénédicte; Cotillard, Aurélie; Atassi, Fabrice; Amour, Julien; Leprince, Pascal; Dutour, Anne; Clément, Karine; Hatem, Stéphane N.

doi:10.1093/eurheartj/eht099

Cited by 480 publications

(380 citation statements)

References 37 publications

Supporting

Mentioning

329

Contrasting

Unclassified

Order By: Relevance

“…In fact, in line with other fat depots [56,57], not only extracellular matrix proteins are remarkably increased in EAT in cardiac pathological conditions [58], but EAT may also induce fibrosis in the neighboring myocardium through the secretion of profibrotic mediators including inflammatory cytokines, growth factors and matrix metalloproteinases [59,60] (Fig. 1).…”

Section: The Emerging Role Of Eat In Cardiac Arrhythmiassupporting

confidence: 55%

“…Among the EAT-secreted factors, activin A resulted one of the main potential mediators of the profibrotic effect of EAT secretome on atrial myocardium [59]. Of note, activin A concentration in the EAT secretome is highly variable, with higher levels in predisposing conditions for atrial arrhythmias, such as heart failure [59], obesity and type 2 diabetes [60].…”

Section: The Emerging Role Of Eat In Cardiac Arrhythmiasmentioning

confidence: 99%

See 1 more Smart Citation

Epicardial adipose tissue: at the heart of the obesity complications

Guglielmi

Sbraccia

2017

Acta Diabetol

Self Cite

View full text Add to dashboard Cite

In recent years, the anatomic and functional contiguity of epicardial adipose tissue (EAT) to myocardium and coronary arteries has gained increasing interest for its potential pathogenetic role in obesity-related cardiac diseases. Besides its known and attributed biochemical cardioprotective properties, it is becoming evident that, in metabolic disease states, EAT-secreted bioactive molecules may play an important role in the pathogenesis of coronary artery disease and cardiac arrhythmias. EAT-derived inflammatory cytokines and reactive oxidative species may, indeed, play a part in the development of a local proatherogenic milieu by paracrine and vasocrine mechanisms of interaction. In addition, initial clinical and in vitro studies have pointed out that EAT could be a determinant of the substrate of atrial fibrillation by contributing to the structural and electrical remodeling of myocardium. This article reviews the current state of knowledge on the association of EAT with cardiac dysfunction and the potential factors mediating the cross talk between this fat depot and the underlying cardiac structures.

show abstract

Section: The Emerging Role Of Eat In Cardiac Arrhythmiassupporting

confidence: 55%

Section: The Emerging Role Of Eat In Cardiac Arrhythmiasmentioning

confidence: 99%

Epicardial adipose tissue: at the heart of the obesity complications

Guglielmi

Sbraccia

2017

Acta Diabetol

Self Cite

View full text Add to dashboard Cite

show abstract

“…Charakterystycznymi cechami tego procesu są aktywacja fibroblastów, zwiększone odkładanie się tkanki łącznej oraz włóknienie [78][79][80]. U pacjentów z AF i towarzyszącymi stanami sprzyjającymi AF stwierdza się również nacieczenie przedsionków tkanką tłuszczową, nacieki zapalne, przerost miocytów, martwicę oraz amyloidozę [81][82][83][84]. Przebudowa strukturalna wywołuje rozkojarzenie elektryczne między pęczkami włókien mięśniowych i miejscową niejednorodność przewodzenia [85], co sprzyja pobudzeniom nawrotnym (re-entry) i podtrzymaniu arytmii [86].…”

Section: Przebudowa Przedsionków a Czynność Kanałów Jonowychunclassified

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Kirchhof

Benussi

Kotecha³

et al. 2016

Kardiol Pol

2,398

4,206

View full text Add to dashboard Cite

“…Obesity not only creates atrial fibrosis 84 , but also increases epicardial fat 84,85 . Furthermore, obesity leads to the infiltration of fat cells into the atrial tissue and to the activation of atrial fat cells, thus modifying atrial electrical function 22,86 , providing a possible mech anism linking obesity and pericardial fat to AF. Therefore, epicardial adipose tissue could be an important health modifier for AF.…”

Section: Fat-cell Infiltration and Activationmentioning

confidence: 99%

“…and mechanisms, and which presents with a variety of symptoms and evolution patterns 2,[15][16][17][18][19][20][21][22][23] . However, none of the current management decisions considers the variable pathophysiology of AF, thereby ignoring the opportunity for tailored, personalized approaches that target the major drivers for AF 24 .…”

mentioning

confidence: 99%

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

et al. 2015

View full text Add to dashboard Cite

Despite the important advances that have enabled better stroke prevention in atrial fibrillation (AF) and more effective maintenance of sinus rhythm over the past decades, a large unmet need to improve the prevention and treatment of AF remains. Mortality for AF remains at 3.5% per year, and death is often experienced as sudden death or as a result of heart failure 1,2 . Each year, approximately 20% of patients with AF need to be hospitalized 3,4 , and stroke occurs in 1.5% of patients with AF who are receiving anticoagulant drugs 5 . Furthermore, more than half of the patients with AF are symptomatic despite adequate anticoagulation and rate control 4,6 . In view of the projected increase in the incidence and prevalence of AF 7-9 , as well as the substantial burden of death and dis ability that is still associated with this condition 10 , the status quo is unacceptable.Current management of patients with AF comprises treatment of the accompanying cardiovascular conditions, oral anticoagulation, rate control -with medications that slow atrioventricular nodal recovery or, rarely, with atrioventricular nodal ablation -and rhythm-control therapy with antiarrhythmic drugs, electrical cardioversion, catheter ablation or, at times, AF surgery 11,12 . Unfortunately, most of these current approaches are disconnected from our understanding of the major mechanisms that cause AF 1,13,14 1,2,7,19,20 Abstract | Despite remarkable advances in antiarrhythmic drugs, ablation procedures, and stroke-prevention strategies, atrial fibrillation (AF) remains an important cause of death and disability in middle-aged and elderly individuals. Unstructured management of patients with AF sharply contrasts with our detailed, although incomplete, knowledge of the mechanisms that cause AF and its complications. Altered calcium homeostasis, atrial fibrosis and ageing, ion-channel dysfunction, autonomic imbalance, fat-cell infiltration, and oxidative stress, in addition to a susceptible genetic background, contribute to the promotion, maintenance, and progression of AF. However, clinical management of patients with AF is currently guided by stroke risk parameters, AF pattern, and symptoms. In response to this apparent disconnect between the known pathophysiology of AF and clinical management, we propose a roadmap to develop a set of clinical markers that reflect the major causes of AF in patients. Thereby, the insights into the mechanisms causing AF will be transformed into a format that can underpin future personalized strategies to prevent and treat AF, ultimately informing better patient care.230 | APRIL 2016 | VOLUME 13 www.nature.com/nrcardio CONSENSUS STATEMENT © 2 0 1 6 M a c m i l l a n P u b l i s h e r s L i m i t e d . A l l r i g h t s r e s e r v e d .

show abstract

Human epicardial adipose tissue induces fibrosis of the atrial myocardium through the secretion of adipo-fibrokines

Abstract: This study provides the first evidence that the secretome from EAT promotes myocardial fibrosis through the secretion of adipo-fibrokines such as Activin A.

Cited by 480 publications

References 37 publications

Epicardial adipose tissue: at the heart of the obesity complications

Epicardial adipose tissue: at the heart of the obesity complications

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

Contact Info

Product

Resources

About