Increased reactive oxygen species production in epicardial adipose tissues from coronary artery disease patients is associated with brown-to-white adipocyte trans-differentiation

Dozio, Elena; Vianello, Elena; Briganti, Silvia; Fink, Bruno; Malavazos, Alexis Elias; Scognamiglio, Elisabetta Thea; Dogliotti, Giada; Sigrüener, Alexander; Schmitz, Gerd

doi:10.1016/j.ijcard.2014.04.045

Cited by 34 publications

(33 citation statements)

References 9 publications

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“…Recent studies have also reported that the increased oxidative stress characterizing EAT of CAD patients is capable of promoting transdifferentiation of brown to white adipocytes [47] and that an increase in 'brown' features of EAT could predict the stability of coronary atheromas in humans [48]. These data support the hypothesis that the presence of adipocytes with brown features in EAT might also contribute to render the local environment proatherogenic.…”

Section: The Clinical Relevance Of Eat In Coronary Artery Diseasesupporting

confidence: 59%

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: The Clinical Relevance Of Eat In Coronary Artery Diseasesupporting

confidence: 59%

Epicardial adipose tissue: at the heart of the obesity complications

Guglielmi

Sbraccia

2017

Acta Diabetol

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“…2). In support of this theory is evidence that the EAT of individuals with CAD is associated with a brown-to-white trans-differentiation characterised by significant decreases in thermogenic genes and upregulation of white adipogenesis [66]. This brown-to-white phenotype is associated with a significant increase in EAT reactive oxygen species production [66] whilst the EAT transcriptome is also characterised by markers of inflammation [67].…”

Section: Cardiac and Vascular Adipose Tissue Dysfunctionmentioning

confidence: 94%

‘Browning’ the cardiac and peri-vascular adipose tissues to modulate cardiovascular risk

Aldiss

Davies

Woods

et al. 2017

International Journal of Cardiology

121

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Excess visceral adiposity, in particular that located adjacent to the heart and coronary arteries is associated with increased cardiovascular risk. In the pathophysiological state, dysfunctional adipose tissue secretes an array of factors modulating vascular function and driving atherogenesis. Conversely, brown and beige adipose tissues utilise glucose and lipids to generate heat and are associated with improved cardiometabolic health. The cardiac and thoracic perivascular adipose tissues are now understood to be composed of brown adipose tissue in the healthy state and undergo a brown-to-white transition i.e. during obesity which may be a driving factor of cardiovascular disease. In this review we discuss the risks of excess cardiac and vascular adiposity and potential mechanisms by which restoring the brown phenotype i.e. “re-browning” could potentially be achieved in clinically relevant populations.

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“…However, the source of ACE and BK was unclear, and EAT may contribute to their accumulation in the pericardial fluid. Higher levels of reactive oxygen species were observed in the EAT of CAD patients21. In severe CAD subjects, the transcriptional level of gene sets related to intracellular trafficking, proliferation/transcription regulation, protein catabolism, innate immunity/lectin pathway, and ER stress were downregulated30.…”

Section: Discussionmentioning

confidence: 93%

“…showed that in patients with CAD, the expression levels of brown fat like genes in EAT was correlated with circulating lipid levels20, which might partially provide clues for the way that EAT affects the progression of CAD. Reactive oxygen species production also remarkably increased in EAT of CAD patients21. Nevertheless, further basic research were needed to clarify more sophisticated functions and pathological changes of EAT in ICM patients.…”

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confidence: 95%

Aberrant Epicardial Adipose Tissue Extracellular Matrix Remodeling in Patients with Severe Ischemic Cardiomyopathy: Insight from Comparative Quantitative Proteomics

Jiang

Zeng

et al. 2017

Sci Rep

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There is ample evidence indicating that epicardial adipose tissue (EAT) volume and thickness is positively associated with coronary artery disease (CAD). However, the exact pathological changes in the human EAT after myocardial ischemia remains largely unclear. In the current study, we applied a comparative quantitative proteomics to elucidate the altered biological processes in the EAT of ischemic cardiomyopathy (ICM) patients. A total of 1649 proteins were successfully quantified in our study, among which 165 proteins were significantly changed (ratio <0.8 or >1.2 fold and p < 0.05 in both repetitions) in EAT of ICM individuals. Gene ontology (GO) enrichment analysis revealed that cardiac structure and cellular metabolism were over-represented among these regulated proteins. The hypertrophic cardiomyopathy, adrenergic signaling in cardiomyocytes, extracellular matrix (ECM)-receptor interaction, phagosome, Glycolysis/Gluconeogenesis, and PPAR signaling pathway were highlighted by the KEGG PATHWAY analysis. More importantly, we found that the proteins responsible for extracellular matrix organization were dramatically increased in EAT of ICM patients. In addition, the picrosirius red (PSR) staining results showed that the collagen fiber content was prominently increased, which indicated the EAT of ICM individuals underwent extracellular matrix remodeling and ERK1/2 activation maybe responsible for these pathological changes partially.

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Increased reactive oxygen species production in epicardial adipose tissues from coronary artery disease patients is associated with brown-to-white adipocyte trans-differentiation

Cited by 34 publications

References 9 publications

Epicardial adipose tissue: at the heart of the obesity complications

Epicardial adipose tissue: at the heart of the obesity complications

‘Browning’ the cardiac and peri-vascular adipose tissues to modulate cardiovascular risk

Aberrant Epicardial Adipose Tissue Extracellular Matrix Remodeling in Patients with Severe Ischemic Cardiomyopathy: Insight from Comparative Quantitative Proteomics

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