Monocyte-platelet cross-talk in peripheral artery disease—how much does the pathogenesis of atherosclerosis depend on anatomical location?

Atherosclerosis results from a complex interaction between leucocytes (primarily monocytes), endothelial cells, endothelial shear stress and platelets. Vascular remodelling is influenced by traditional risk factors and also mediated by cytokines (1). Monocytes are mononuclear cells of myeloid origin and represent about six percent of the total leukocyte population (2). Current nomenclature divides them into three (functionally diverse) subsets; Mon1 (CD14++CD16, formerly known as classical) represent about 85% of monocyte population, Mon2 (CD14++CD16+, formerly intermediate), about 5% and Mon3 (CD14+CD16++, previously non-classical), about 10% (3). Monocytes play a significant role in the pathogenesis of atherogenesis.