Abstract
Background: Genome wide association studies shows SORT1 expression to affect lipid metabolism and thus identifies it as a risk gene for coronary artery disease (CAD). Higher circulating levels of Sortilin in patients with atherosclerosis is reported. However very little is known about its expression in patients with CAD. In hepatocytes, Sortilin interacts with PCSK9 in Trans Golgi network and helps its secretion from liver. In macrophages, Sortilin promotes LDL uptake, form cell formation and atherosclerosis.
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