Abstract
LOX-1 may play important roles in oxLDL-induced apoptosis of intimal VSMC. Although multiple molecules may be involved in oxLDL uptake in macrophages, SR-PSOX might contribute to oxLDL-induced accumulation of cholesteryl ester in macrophages. These biologic functions of LOX-1 and SR-PSOX may stimulate atherosclerotic plaque rupture. Future studies with functional blockade of these novel scavenger receptors in appropriate animal models in vivo may elucidate the true roles of these molecules. In the future, plasma levels of soluble LOX-1, and possibly SR-PSOX/CXCL16, might provide us with novel insights as risk markers for atherosclerotic progression and the plaque rupture.
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