Figure 1.

Cell-specific contribution of autophagy in atherogenesis. Autophagy governs homeostasis of cell types involved in all stages of atherogenesis. In endothelial cells (ECs), autophagy enhances nitric oxide (NO) bioavailability and prevents endothelial dysfunction and inflammatory activation, for example by lowering expression of adhesion molecules such as ICAM-1, VCAM-1, and PECAM-1. Autophagy regulates proliferation and migration of vascular smooth-muscle cells (VSMCs), contributes to their phenotypic switch, and regulates their lipid metabolism. Finally, autophagy machinery is involved in immune cell differentiation, proliferation, and lipid metabolism. Moreover, by affecting the adaptive immune system, it also contributes to the immune response to oxLDL epitopes and differentiation of T-cell subsets. LDL, low-density lipoproteins; Mac^AIR, aortic intimal resident macrophages.