Fig. 10: Proposed model of the molecular mechanism of action of NMVs in atherosclerosis.
From: Neutrophil microvesicles drive atherosclerosis by delivering miR-155 to atheroprone endothelium
High fat diet increases the level of circulating NMVs (i) that preferentially adhere to atheroprone regions of arteries (ii) where they become internalised by endothelial cells (iii). Delivery of miR-155 to the endothelial cells downregulates BCL6, leading to an increase in NF-κB expression and subsequent inflammatory activation. This results in an increase in the number of monocytes recruited to the vessel wall and enhanced atherosclerotic plaque formation.
