Figure 2.

Examples of autocrine/paracrine interactions of inflammatory mediators in vascular remodeling in atherosclerosis. Inflammatory mediators can act in an autocrine manor, CCL2 and CCL5 for example activate VSMCs to undergo phenotypical changes in atherosclerosis. EC and VSMC derived CCL2 can further foster cross-talk between them promoting remodeling. CCL2 from ECs triggers synthetic differentiation of VSMCs and CCL2 from VSMCs promotes monocyte recruitment. Alternatively, mediators like interlukin-1β, expressed by dendritic cells (DCs) and natural killer (NKs) cells promote the upregulation of adhesion molecule expression by ECs, transmigration of circulating leukocytes and VSMC proliferation in a paracrine fashion. IL-1β in addition can act upon macrophages to promote IL-1β secretion in an autocrine manner. IL-6 secreted by ECs, monocytes, T cells, neutrophils and VSMCs promotes adhesion molecule expression by ECs as well as transmigration of circulating immune cells into the atherosclerotic plaque (this figure was made with Biorender.com).