Loss of Spry1 in vascular smooth muscle cells promotes hypercholesterolemiainduced VSMC phenotypic transitions and regulates atherogenesis

Atherosclerosis is an inflammatory disease characterized by arterial wall thickening and plaque accumulation, and is a major cause of death worldwide. Vascular smooth muscle cells (VSMC), which have the unique ability to transition from mature contractile cells to myofibroblasts and macrophagelike foam cells, and adopt a proinflammatory state contribute to atherogenic microenvironment (1). We aimed to investigate how Spry1, a regulator of receptor tyrosine kinase signaling, affects hypercholesterolemia induced plaque formation in mice by manipulating Spry1 expression specifically in VSMC