Key result
Pericardial fluid EVs from CAD patients alter lipid profiles in human coronary artery endothelial cells.
Why the study?
It was not understood how factors in the pericardial fluid of patients with CAD influence the coronary artery endothelium lipidome.
Do pericardial fluid-derived small extracellular vesicles from patients with CAD alter the lipidome of human coronary artery endothelial cells compared to non-CAD patients?
Observational (n=6)
Do pericardial fluid-derived small extracellular vesicles from patients with CAD alter the lipidome of human coronary artery endothelial cells compared to non-CAD patients?
Answers are grounded in this paper and cite their sources.
Small extracellular vesicles derived from the pericardial fluid of CAD patients uniquely alter the lipid profile of human coronary artery endothelium, suggesting a potential mechanism in the pathophysiology of ischemic heart disease.
Background: To date, we have lacked an understanding of how factors in the pericardial fluid (PF) of patients with coronary artery disease (CAD) can influence the lipidome of coronary artery endothelium. This study explores the impact of PF-derived extracellular vesicles (EVs) on the lipidome of human coronary artery endothelial cells (HCAECs) in patients with CAD. Methods: In this observational study, PF was collected from patients with CAD (n = 3) and without CAD (n = 3). PF-derived small EVs were isolated and characterized using microfluidic resistive pulse sensing. HCAECs were exposed to these EVs, and untargeted liquid chromatography-mass spectrometry was subsequently used to determine the lipidome of the HCAECs. In silico analysis was used to evaluate changes in lipid species and classes. Results: A total of 1043 lipid species were identified in untreated HCAECs and HCAECs treated with PF-derived small EVs. The predominant lipid types were glycerophospholipids, glycerolipids, and sphingolipids. Quantification of individual lipid classes showed HCAECs treated with PF EVs showed reduced summed intensities of lysophosphatidylglycerols and diacylglycerophosphoinositols compared to untreated controls. Treatment with PF EVs derived from Non-CAD patients led to an increase in sphingoid bases, whereas this effect was not observed with CAD-derived PF EVs. Both Non-CAD and CAD PF EV treatments resulted in elevated prenol lipids compared to controls. Conclusions: We identify that small EVs isolated from the PF of patients with CAD alter the lipid profile and metabolism of human coronary artery endothelium. Future studies should determine whether such changes can contribute to the pathophysiology of ischemic heart disease.
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Hassanabad et al. (2025) conducted an observational in Coronary artery disease (n=6). Pericardial fluid-derived small extracellular vesicles vs. Untreated controls and non-CAD derived extracellular vesicles was evaluated on Lipidome of human coronary artery endothelial cells. Exposure of human coronary artery endothelial cells to pericardial fluid-derived small extracellular vesicles from CAD patients altered their lipid profile among 1043 identified lipid species.
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