CCL2 and atherosclerosis: Hypoxia and HIF-1 may participate in the pathogenesis of atherosclerosis by leading to the production of factors that elevate synthesis (3-hydroxy-3-methylglutaryl-CoA reductase, Lipin1) and uptake (CD36, fatty‐acid‐binding proteins, LDLR, VLDLR) of lipids, recruit inflammatory cells (chemokine monocyte chemoattractant protein-1 MCP-1/CCL2), and promoting angiogenesis (VEGF) within plaques.