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High-throughput screen identifies metabolite regulators of endothelial function.
Sci. Rep. 16:30527 (2026)
Endothelial cells (ECs) line blood vessels, regulate organ homeostasis, and their dysfunction is central to the development of cardiovascular diseases. Metabolites are critical regulators of EC health and function, yet only a limited number of metabolites that impact ECs have been identified. Here, we undertook a high-throughput screen of 884 metabolites and common drugs found in human biofluids to systematically identify compounds that impact barrier function in primary human umbilical vein ECs (HUVECs). Seven metabolites that deregulate vascular barrier function without causing cell death were shortlisted. These include (-)-epigallocatechin gallate, (±)-3-methyl-2-oxovaleric acid, taurocholic acid, myricetin, meloxicam, hesperetin and trans-3-indoleacrylic acid. These metabolites elicited differential effects on HUVECs, coronary artery ECs and pulmonary ECs. Transcriptional profiling revealed that each of the seven metabolites triggered distinct transcriptional responses in ECs, suggesting distinct mechanisms triggering EC barrier disruption. Notably, trans-3-indoleacrylic acid deregulated VE-cadherin junctions and increased EC sprouting, suggesting a potential role in angiogenesis. Together, these results provide a screening resource for metabolite-endothelial interactions and identify candidate circulating metabolites that regulate endothelial function.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Endothelial Function ; Endothelial Barrier Function ; Circulating Metabolites ; Metabolite Screening ; Human Umbilical Vein Endothelial Cells ; Angiogenesis ; Endothelial Sprouting ; Epigallocatechin Gallate ; Taurocholate ; Myricetin ; Meloxicam ; Hesperetin ; Endothelial Dysfunction ; Cardiovascular Disease ; Transcriptional Response; L-carnitine; Dysfunction; Permeability; Cells; Risk; Cyclooxygenase-2; Modulation; Mechanisms; Resistance; Oxygen
ISSN (print) / ISBN
2045-2322
e-ISSN
2045-2322
Journal
Scientific Reports
Quellenangaben
Volume: 16,
Issue: 1,
Article Number: 30527
Publisher
Springer
Publishing Place
London
Reviewing status
Peer reviewed
Institute(s)
Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG)
Grants
Deutsche Forschungsgemeinschaft