Role of epicardial adipose tissue NPR-C in acute coronary syndrome

Inflammation is widely known to play a key role in the development and progression of cardiovascular diseases. It is becoming increasingly evident that obesity is linked to many proinflammatory and obesity-associated cardiovascular conditions (e.g., metabolic syndrome, acute coronary syndrome, and congestive heart failure). It has been observed that adipokines play an increasingly large role in systemic and local inflammation. Therefore, adipose tissue may have a more important role than previously thought in the pathogenesis of several disease types. This review explores the recently described role of adiponectin as an immunomodulatory factor and how it intersects with the inflammation associated with both cardiovascular and autoimmune pathologies.

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Could Epicardial Adipose Tissue Thickness by Echocardiography Be Correlated with Acute Coronary Syndrome Risk Scores

Echocardiography ◽

10.1111/echo.12276 ◽

2013 ◽

Vol 30 (10) ◽

pp. 1130-1134 ◽

Cited By ~ 7

Author(s):

Burak Altun ◽

Yucel Colkesen ◽

Emine Gazi ◽

Hakan Tasolar ◽

Ahmet Temiz ◽

...

Keyword(s):

Acute Coronary Syndrome ◽

Adipose Tissue ◽

Epicardial Adipose Tissue ◽

Risk Scores ◽

Tissue Thickness ◽

Coronary Syndrome ◽

Epicardial Adipose Tissue Thickness

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Imbalance Between Interleukin-1β and Interleukin-1 Receptor Antagonist in Epicardial Adipose Tissue Is Associated With Non ST-Segment Elevation Acute Coronary Syndrome

Frontiers in Physiology ◽

10.3389/fphys.2020.00042 ◽

2020 ◽

Vol 11 ◽

Cited By ~ 4

Author(s):

Valentina Parisi ◽

Laura Petraglia ◽

Serena Cabaro ◽

Vittoria D’Esposito ◽

Dario Bruzzese ◽

...

Keyword(s):

Acute Coronary Syndrome ◽

Adipose Tissue ◽

Receptor Antagonist ◽

Epicardial Adipose Tissue ◽

Interleukin 1 ◽

Interleukin 1Β ◽

St Segment Elevation ◽

Coronary Syndrome ◽

Interleukin 1 Receptor Antagonist ◽

St Segment

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Epicardial adipose tissue thickness and acute coronary syndrome: A matter of how much or how?

International Journal of Cardiology ◽

10.1016/j.ijcard.2015.06.168 ◽

2015 ◽

Vol 199 ◽

pp. 8-9 ◽

Cited By ~ 3

Author(s):

Gianfranco Aprigliano ◽

Lea Scuteri ◽

Ida Iafelice ◽

Laura Li Volsi ◽

Besart Cuko ◽

...

Keyword(s):

Acute Coronary Syndrome ◽

Adipose Tissue ◽

Epicardial Adipose Tissue ◽

Tissue Thickness ◽

Coronary Syndrome ◽

Epicardial Adipose Tissue Thickness

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Increased expression and secretion of resistin in epicardial adipose tissue of patients with acute coronary syndrome

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00617.2009 ◽

2010 ◽

Vol 298 (3) ◽

pp. H746-H753 ◽

Cited By ~ 65

Author(s):

Silvia Langheim ◽

Lorella Dreas ◽

Lorenzo Veschini ◽

Francesco Maisano ◽

Chiara Foglieni ◽

...

Keyword(s):

Acute Coronary Syndrome ◽

Adipose Tissue ◽

Endothelial Cell ◽

Protein Secretion ◽

Epicardial Adipose Tissue ◽

Cell Permeability ◽

Coronary Syndrome ◽

Endothelial Cell Permeability ◽

Stable Cad

The purpose of this study was to test the hypothesis that specific epicardial adipose tissue (EAT) proinflammatory adipokines might be implicated in acute coronary syndrome (ACS). We compared expression and protein secretion of several EAT adipokines of male ACS with those of matched stable coronary artery disease (CAD) patients and controls with angiographically normal coronary arteries. The effect of supernatant of cultured EAT on endothelial cell permeability in vitro was also evaluated in the three study groups. EAT of ACS patients showed significantly higher gene expression and protein secretion of resistin than patients with stable CAD. Interleukin-6, plasminogen activator inhibitor-1, and monocyte chemoattractant protein-1 genes were also significantly overexpressed in ACS compared with the control group but not when compared with stable CAD. Immunofluorescence of EAT sections revealed a significantly greater number of CD68+ cells in ACS patients than stable CAD and control groups. The permeability of endothelial cells in vitro was significantly increased after exposure to supernatant of cultured EAT from ACS, but not control or stable CAD groups, and this effect was normalized by anti-resistin antiserum. We found that EAT of patients with ACS is characterized by increased expression and secretion of resistin and associated with increased in vitro endothelial cell permeability.

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