Time-dependent specific molecular signatures of inflammation and remodelling are associated with Trimethylamine-N-oxide (TMAO)-induced endothelial cell dysfunction
Cardiovascular diseases (CVDs) are leading causes of death worldwide. Endothelial dysfunction is a critical initiating factor contributing to CVDs, which progression involves the gut microbiome-derived metabolite Trimethylamine N-oxide (TMAO). Here, we aim to clarify the time-dependent pathways by which TMAO mediates endothelial dysfunction. Overall design: We performed transcriptomics and metabolomics analyses on human microvascular endothelial cells (HMEC-1) treated with TMAO. Differentially expressed genes (DEG) and gene set enrichment analysis (GSEA) followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses allowed the identification of specific molecular pathways. Cell viability and reactive oxygen species (ROS) generation were also evaluated.