Human epicardial adipose tissue has a specific transcriptomic signature depending on its anatomical peri-atrial, peri-ventricular, or peri-coronary location

Gaborit, Bénédicte; Venteclef, Nicolas; Ancel, Patricia; Pelloux, Véronique; Gariboldi, Vlad; Leprince, Pascal; Amour, Julien; Hatem, Stéphane N.; Jouve, Élisabeth; Dutour, Anne; Clément, Karine

doi:10.1093/cvr/cvv208

Cited by 168 publications

(135 citation statements)

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“…In particular, the peri-coronary EAT resulted more closely involved in atherotic plaques formation, expressing genes involved in cell proliferation and in metabolism of sphingolipids which are lipid components of atheromas capable of promoting oxidized LDL and VLDL retention in the sub-endothelial space. In contrast, peri-ventricular EAT was more strictly linked to genes regulating inflammatory pathways, whereas the genes most up-regulated by periatrial EAT were implicated in energy metabolism, cardiomyocyte contractility and intracellular calcium signaling [64].…”

Section: Does Eat Location Matter?mentioning

confidence: 83%

Epicardial adipose tissue: at the heart of the obesity complications

Guglielmi

Sbraccia

2017

Acta Diabetol

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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.

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Section: Does Eat Location Matter?mentioning

confidence: 83%

Epicardial adipose tissue: at the heart of the obesity complications

Guglielmi

Sbraccia

2017

Acta Diabetol

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“…В исследовании, проведенном во Франции в 2014 г., Gaborit B. с коллегами продемонстрировали по-вышенную экспрессию ЭЖТ генов ремоделирования экс-трацеллюлярного матрикса, кодирующих структуру коллагена IV и VI типов, тромбоспондина 3, ламини-на-α2, фибронектина 1 [24].…”

Section: фиброзunclassified

“…миокарда предсердий В эксперименте Gaborit B. с коллегами было дока-зано, что только в ЭЖТ, окружающей предсердия, на-блюдается повышение экспрессии генов окислительного фосфорилирования циклооксигеназы, АТФазы, кле-точной адгезии (ANKRD1, TNC, COL4A4) и кальциевых сигнальных путей (SERCA1, CAMK2B, CAMK2D, NCX2), что может быть связано с развитием ФП [24].…”

Section: прямое влияние на мышечную активностьunclassified

Pathogenic Mechanisms of Atrial Fibrillation in Obesity

Drapkina

Nikolaeva

2016

Racionalʹnaâ farmakoterapiâ v kardiologii

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По оценкам Всемирной Организации Здраво-охранения ожирение в 21 веке приняло характер эпи-демии, с каждым годом число больных ожирением не-изменно растет. Современный образ жизни прово-цирует изменения в режиме труда и отдыха, в харак-тере питания и образе жизни, поэтому ожирение и из-быточную массу тела можно считать проблемами со-временности. Ожирение является доказанным фак-тором риска развития сердечно-сосудистых заболе-ваний [1].Фибрилляция предсердий (ФП) является одной из наиболее встречающихся аритмий. Число больных ФП по разным оценкам составляет от 1 до 5% населе-ния. Этот тип аритмии опасен своими осложнениями в виде системных тромбоэмболий, в том числе тром-боэмболического инсульта. Ожирение, как независи-мый фактор риска развития ФП, повышает вероятность ее возникновения на 50%. Точные механизмы влияния избыточной массы тела на развитие аритмий до кон-ца не установлены, большинство исследований в этом Фибрилляция предсердий (ФП) является одной из наиболее распространенных аритмий. Ее появление приводит к снижению качества жиз-ни и уменьшению ее продолжительности за счет тромбоэмболических осложнений. Ожирение способствует структурному и электрическо-му ремоделированию миокарда предсердий, что приводит к возникновению эктопических фокусов в устьях легочных вен и нарушению нор-мального электрического проведения по предсердиям. К основным механизмам формирования аритмогенного субстрата относят системное воспаление, фиброз миокарда, перегрузку кардиомиоцитов ионами Na + и Са 2+ , накопление в клетках недоокисленных продуктов метабо-лизма, дисбаланс вегетативной регуляции. Ассоциированные с ожирением артериальная гипертензия, инсулинорезистентность и синдром обструктивного апноэ сна повышают риск возникновения и прогрессирования аритмии. Исследование патогенетических механизмов воз-никновения ФП при ожирении необходимо для разработки новых стратегий ее профилактики и создания более эффективных методов лече-ния у данной группы пациентов. Патогенетические механизмы развития фибрилляции предсердий при ожиренииКлючевые слова: фибрилляция предсердий, ожирение, воспаление, фиброз. Atrial fibrillation (AF) is one of the most common arrhythmias. It reduces quality of life and its duration due to thromboembolic complications. Obesity contributes to the structural and electrical remodeling of atrial myocardium. This leads to occurrence of ectopic foci in the mouths of the pulmonary veins and the disruption of normal electrical conduction in the atria. Systemic inflammation, myocardial fibrosis, cardiomyocyte overload by Na + and Ca 2+ ions, accumulation in the cells of unoxidized metabolic products, imbalance of the autonomic regulation are considered as the main mechanisms of arrhythmogenic substrate formation. Hypertension, insulin resistance, and obstructive sleep apnea, associated with obesity, increase the risk of development and progression of the arrhythmia. Study of pathogenetic mechanisms of AF in obesity is necessary to develop new strategies for its prevention and the creation of more effective methods ...

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“…Of note, these biological variations are depot specific. Genome,15 16 transcriptome,17 proteome18 and mriRNome19-wide expression analyses have identified significant phenotypic differences between epicardial adipose tissue (EAT) and subcutaneous AT (SAT) in patients with CAD. Compared with SAT, EAT is characterised by higher expression of pro-inflammatory (tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin 1- β (IL1-β)), pro-oxidant (NADPH-oxidase, superoxide dismutase-2, catalase, glutathione S-transferase P, protein disulfide isomerase) and angiogenic (vascular endothelial growth factor receptor 1, endothelin 1, angiotensin II receptor 1)-regulatory genes as well as greater infiltration by immune cells, particularly M1 proinflammatory macrophages 16 18 20.…”

Section: Introductionmentioning

confidence: 99%

Perivascular adipose tissue and coronary atherosclerosis

Mâncio

Oikonomou

Antoniades

2018

Heart

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Adipose tissue (AT) is no longer viewed as a passive, energy-storing depot, and a growing body of evidence supports the concept that both quantitative and qualitative aspects of AT are critical in determining an individual's cardiometabolic risk profile. Among all AT sites, perivascular AT (PVAT) has emerged as a depot with a distinctive biological significance in cardiovascular disease given its close anatomical proximity to the vasculature. Recent studies have suggested the presence of complex, bidirectional paracrine and vasocrine signalling pathways between the vascular wall and its PVAT, with far-reaching implications in cardiovascular diagnostics and therapeutics. In this review, we first discuss the biological role of PVAT in both cardiovascular health and disease, highlighting its dual pro-atherogenic and anti-atherogenic roles, as well as potential therapeutic targets in cardiovascular disease. We then review current evidence and promising new modalities on the non-invasive imaging of epicardial AT and PVAT. Specifically, we present how our expanding knowledge on the bidirectional interplay between the vascular wall and its PVAT can be translated into novel clinical diagnostics tools to assess coronary inflammation. To this end, we present the example of a new CT-based method that tracks spatial changes in PVAT phenotype to extract information about the inflammatory status of the adjacent vasculature, highlighting the numerous diagnostic and therapeutic opportunities that arise from our increased understanding of PVAT biology.

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Human epicardial adipose tissue has a specific transcriptomic signature depending on its anatomical peri-atrial, peri-ventricular, or peri-coronary location

Abstract: This study opens new perspectives in understanding the physiology of human EAT and its local interaction with neighbouring structures.

Cited by 168 publications

References 58 publications

Epicardial adipose tissue: at the heart of the obesity complications

Epicardial adipose tissue: at the heart of the obesity complications

Pathogenic Mechanisms of Atrial Fibrillation in Obesity

Perivascular adipose tissue and coronary atherosclerosis

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