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This editorial refers to ‘Insulin resistance aggravates atherosclerosis by reducing vascular smooth muscle cell survival and increasing CX3CL1/CX3CR1 axis’ by S. Martinez-Hervas et al. , doi:10.1093/cvr/cvu115. The mechanisms driving accelerated atherosclerosis in insulin-resistant (IR) conditions, such as Type 2 diabetes and the metabolic syndrome, are incompletely understood. Clarifying such pathways is of paramount importance in view of the epidemic spread of obesity and diabetes, and in order to devise novel therapeutic approaches to counter cardiovascular disease globally. IR develops classically in metabolically active tissues (such as the liver, muscle, and fat), but the vasculature can also show signs of IR,1 with impairment in the Erk and Akt pathways.Many cell types are involved in the atherogenetic process and complex cross-talks take place within the atherosclerotic plaque. Vascular smooth muscle cells (VSMCs) and monocyte–macrophage lineage cells are two major players provided with both protective and pathogenic functions. VSMC proliferation promotes plaque growth, but also forms the fibrous cap of the atheroma, a thick and resistant shield against plaque rupture and thrombosis. However, VSMCs from human atherosclerotic vessels are senescent and intrinsically prone to apoptosis.2,3 In fact, when VSMCs undergo apoptosis, atherosclerosis accelerates, and plaques become unstable …

Vascular smooth muscle cells and monocyte–macrophages accomplice in the accelerated atherosclerosis of insulin resistance states