OF PLAQUES AND STONES: THE SR-B1
cardiovascular disease, while this risk is inversely proportional to plasma HDL-cholesterol levels. On the other hand, (SCAVENGER RECEPTOR CLASS B, TYPE 1) secretion of excessive free cholesterol into bile is critical to Kozarsky KF, Donahee MH, Rigotti A, Iqbal SN, Edelman the formation of cholesterol gallstones. Biliary free choles-ER, Krieger M. Overexpression of the HDL Receptor SR-B1 terol is derived principally from the cholesterol contained alters plasma HDL and bile cholesterol levels. Reprinted with in circulating lipoproteins, and not from cholesterol synthepermission. Nature 1997;387(6631):414-417. sized within the liver. 1 Thus, hepatocellular uptake of cholesterol from plasma lipoproteins across the basolateral (si-ABSTRACT nusoidal) plasma membrane, and subsequent trafficking of cholesterol to the apical (canalicular) plasma membrane for The risk of atherosclerosis, a leading cause of cardiovassecretion into bile, are critical for determining the risk of tein in hepatobiliary lipid transport. FASEB J 1997;11:19-28. 19. Wang DQH, Paigen B, Carey MC. Phenotypic characterization of Lith risk of cholesterol gallstone formation, regardless of the genes that determine susceptibility to cholesterol cholelithiasis in inbred mechanism of action. The recent cloning of the human homice. Physical-chemistry of gallbladder bile. J Lipid Res 1997;38:1395mologue to mSR-B1, the ''human CD36 and LIMPII analo-1411.
gous-1'' (CLA-1) receptor, is particularly relevant in this re-20. Murao K, Terpstra V, Green SR, Kondratenko N, Steinberg D, Quehen- berger O. Characterization of CLA-1, a human homologue of rodent gard. 20 Clearly, the opportunity now beckons for improved scavenger receptor BI, as a receptor for high density lipoprotein and understanding and management of atherosclerotic cardiovasapoptotic thymocytes.