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Inflamed epicardial fat (EAT) accumulation around the myocardium and coronaries is a risk factor for cardiovascular disease. Glucagon-like peptide receptor-agonists 1 improves the insulin response and reduces EAT thickness. We aimed to demonstrate the effect of semaglutide on proinflammatory epicardial adipogenesis with paracrine effects on cardiomyocytes. Biopsies or isolated stromal cells from subcutaneous adipose tissue and EAT of 67 patients undergoing open-heart surgery were studied by real-time quantitative polymerase chain reaction, proteomics, and metabolic assays. Adipogenesis assay and paracrine effect over atrial cardiomyocytes determined that semaglutide treatment modulates proinflammatory adiposity markers FABP4 and sPLA2 in epicardial adipogenesis with a paracrine effect in atrial cardiomyocytes.
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http://dx.doi.org/10.1016/j.jacbts.2025.03.009 | DOI Listing |
Cells
August 2025
Institute for Physiology and Pathophysiology, Department of Pathophysiology, Johannes Kepler University Linz, Krankenhausstrasse 5, 4020 Linz and Altenberger Strasse 69, 4040 Linz, Austria.
Adipose tissue enlargement in obesity leads to hypoxia, which may promote premature aging. This study aimed to understand the hypoxic response in 3D cultures of SGBS cells, a model for brown-like adipose tissue expressing uncoupling protein 1 (UCP1). Single-nucleus RNA sequencing of SGBS organoids revealed a heterogeneous composition and sub-population-specific responses to hypoxia.
View Article and Find Full Text PDFJACC Basic Transl Sci
June 2025
Translational Cardiology, Health Research Institute of Santiago de Compostela, Santiago de Compostela, Spain; CIBERCV, ISCIII, Madrid, Spain. Electronic address:
Inflamed epicardial fat (EAT) accumulation around the myocardium and coronaries is a risk factor for cardiovascular disease. Glucagon-like peptide receptor-agonists 1 improves the insulin response and reduces EAT thickness. We aimed to demonstrate the effect of semaglutide on proinflammatory epicardial adipogenesis with paracrine effects on cardiomyocytes.
View Article and Find Full Text PDFCirc Arrhythm Electrophysiol
September 2024
Cardiovascular Department, Grupo de Cardiología Traslacional (M.C.-S., X.V.-A., S.E.), IDIS, Santiago de Compostela, Spain.
Background: Adipocyte FABP4 (fatty acid-binding protein 4) is augmented in the epicardial stroma of patients with long-standing persistent atrial fibrillation. Because this molecule is released mainly by adipocytes, our objective was to study its role in atrial cardiomyopathy, focusing our attention on fibrosis, metabolism, and electrophysiological changes. These results might clarify the role of adiposity as a mediator of atrial cardiomyopathy.
View Article and Find Full Text PDFJ Transl Med
July 2024
Centro de Investigación Biomédica en Red en Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
Background: Carbohydrate antigen 125 (CA125) is a proteolytic fragment of MUC-16 that is increased in heart failure (HF) and associated with inflammation, fluid overload, and worse adverse events. Our main objective was to study the expression of CA125 on epicardium and its association with inflammation, adipogenesis, and fibrosis.
Methods: Epicardial fat biopsies and blood were obtained from 151 non-selected patients undergoing open heart surgery.
JAMA Cardiol
May 2024
Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, Massachusetts.
Importance: Epicardial and pericardial adipose tissue (EPAT) has been associated with cardiovascular diseases such as atrial fibrillation or flutter (AF) and coronary artery disease (CAD), but studies have been limited in sample size or drawn from selected populations. It has been suggested that the association between EPAT and cardiovascular disease could be mediated by local or paracrine effects.
Objective: To evaluate the association of EPAT with prevalent and incident cardiovascular disease and to elucidate the genetic basis of EPAT in a large population cohort.