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Scavenger receptor class B member 1 (SR‑B1) is a transmembrane glycoprotein primarily responsible for mediating the selective uptake of cholesteryl esters from high-density lipoproteins into hepatocytes, steroidogenic organs, macrophages, adipose tissue, gut epithelium, and endothelium. It plays a central role in reverse cholesterol transport—the process by which excess peripheral cholesterol is returned via HDLs to the liver for excretion—thereby contributing significantly to cardiovascular health. Beyond its role in lipid metabolism, interaction between HDLs/SR‑B1 also influences endothelial cell signaling pathways involved in vasodilation, anti-apoptosis, proliferation/migration responses. Dysregulation or genetic variants affecting this pathway have been linked with increased risk for coronary artery disease. While direct pharmacological modulation remains experimental at present, it represents an attractive therapeutic strategy for managing dyslipidemia-related disorders[3][4][5].
Drugs targeting this molecule would typically: Enhance or inhibit selective uptake of cholesteryl esters from HDL into hepatocytes/steroidogenic cells via SR-BI-mediated transfer. Modulate reverse cholesterol transport efficiency. Indirect mechanisms include upregulation/downregulation through nuclear hormone receptors affecting gene expression.
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