Atherosclerosis – the build-up of fatty plaques (atheromas) inside arteries – is the primary driver of cardiovascular disease, which accounts for 1 in 3 deaths in the United States. Identifying “atheroprotective” genes that delay atheroma initiation, progression or destabilization might suggest novel therapeutic interventions for atherosclerosis.
Pampee Young, M.D., Ph.D., graduate student Amanda Segedy and colleagues previously identified the candidate atheroprotective gene SPRR3 (small proline-rich repeat protein) as being expressed in vascular smooth muscle cells (VSMCs) of atheroma-bearing arteries, but not healthy arteries. They have now demonstrated that loss of SPRR3 expression in mice leads to increased atheroma burden and increased death of VSMCs. Endothelial cells and blood cells were unaffected by SPRR3 loss.
The findings, reported in the December issue of Arteriosclerosis, Thrombosis, and Vascular Biology, suggest that SPRR3 promotes survival signaling in VSMCs and limits atherosclerosis progression. SPRR3 has great potential as both a tool to explore the function of VSMCs in plaque pathophysiology and as a potential target for therapies to slow atherosclerosis progression.
This research was supported by funding from the Veterans Affairs Merit Award and by the National Institutes of Health (grants RR024975, HL105375, HL057986, DK059637).
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