Nicotine exacerbates endothelial dysfunction and drives atherosclerosis via extracellular vesicle-miRNA.

Based on the findings of our study, strategies preventing or blocking the production of abnormal EVs, particularly monocyte EVs, after nicotine stimulation may protect against atherosclerosis. Moreover, detection of circulating EVs-carried miR-155 expression may reveal the progression of atherosclerosis. On the molecular level, blocking miR-155 biogenesis, which constituted a novel therapeutic approach, may protect against nicotine aggravating atherosclerosis.