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Semaglutide Modulates Proinflammatory Epicardial Adipogenesis With Paracrine Effects on hiPSC-Atrial Cardiomyocytes
Rumeysa Basdas1, José Manuel Martínez-Cereijo2, Ángel L Fernández3
1Translational Cardiology, Health Research Institute of Santiago de Compostela, Santiago de Compostela, Spain; University of Santiago de Compostela, Santiago de Compostela, Spain.
Semaglutide, a glucagon-like peptide receptor agonist, reduces inflammation in epicardial fat (EAT) and impacts atrial cardiomyocytes. This finding offers new insights into cardiovascular disease risk management.
Area of Science:
- Cardiovascular Science
- Metabolic Disease Research
- Adipose Tissue Biology
Background:
- Inflamed epicardial fat (EAT) accumulation is a significant risk factor for cardiovascular disease.
- Glucagon-like peptide receptor agonists improve insulin response and reduce EAT thickness.
Purpose of the Study:
- To investigate the effect of semaglutide on proinflammatory epicardial adipogenesis.
- To assess the paracrine effects of semaglutide on cardiomyocytes.
Main Methods:
- Analysis of subcutaneous adipose tissue and EAT from 67 patients undergoing open-heart surgery.
- Utilized real-time quantitative PCR, proteomics, and metabolic assays.
- Performed adipogenesis assays and paracrine effect studies on atrial cardiomyocytes.
Main Results:
- Semaglutide treatment modulated proinflammatory adiposity markers, including FABP4 and sPLA2, in epicardial adipogenesis.
- Demonstrated a paracrine effect of semaglutide on atrial cardiomyocytes.
Conclusions:
- Semaglutide influences proinflammatory adiposity markers in EAT.
- Semaglutide exhibits paracrine effects on atrial cardiomyocytes, suggesting potential cardiovascular benefits.
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