Semaglutide modulates prothrombotic and atherosclerotic mechanisms, associated with epicardial fat, neutrophils and endothelial cells network
Authors' conclusion
Semaglutide increases endocrine activity of epicardial fat with antithrombotic properties. Moreover, this drug modulates the pro-inflammatory and atherogenic profile induced by the adiposity marker, FABP4, which is also reduced in patients after semaglutide treatment.
Study context
- Population
- Patients undergoing cardiac surgery (EAT and SAT samples); patients treated with semaglutide for 6 months
- Comparison
- Semaglutide treatment
- Outcome
- Effects of semaglutide on EAT, neutrophils and endothelial cells
Main finding
As reported in the abstract
- GLP-1 receptor expressed on fat and neutrophils
- Differential exosome protein cargo on EAT explants after semaglutide
- Semaglutide increased secretion of gelsolin (antithrombotic protein) by EAT
- Semaglutide modulated CD11b on neutrophils, their migration and endothelial adhesion induced by FABP4 or a chemoattractant
Further findings
Plasma markers and immune cell phenotype in patients · 6 months of semaglutide
- Reduction in FABP4 levels, with statistical significance
- 20%
- Increase of neutrophils-CD88
- 80%
Original publication
Semaglutide modulates prothrombotic and atherosclerotic mechanisms, associated with epicardial fat, neutrophils and endothelial cells network. Cardiovasc Diabetol. Published 3 January 2024. doi:10.
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