Lipoprotein receptors and atherosclerosis.
Mammalian cholesterol metabolism is governed by two key features of the steroid nucleus: it is poorly soluble in plasma and it cannot be degraded in animal tissues. Cells which require the lipid import it through their cytoplasmic membranes in the form of solubilized lipid-protein complexes, and a similar export mechanism is essential in order to maintain cellular homoeostasis. The translocation is mediated by high affinity receptors which, under normal circumstances, operate in close synchrony. Changes in the nature of the lipoprotein ligand or of the cell itself may disturb this balance and lead to the pathological sterol accumulation which characterizes atherosclerotic lesions. All body tissues engage in this traffic in cholesterol but the liver is the single most important organ since it has the capacity both to synthesize large quantities of the lipid and to excrete it from the body via a variety of receptors designed to maintain peripheral sterol levels within safe limits.
D001161:Arteriosclerosis / Q000378:metabolism*; D002352:Carrier Proteins; D002784:Cholesterol / Q000378:metabolism; D006801:Humans; D008075:Lipoproteins, HDL; D026503:Low Density Lipoprotein Receptor-Related Protein-1; D016601:RNA-Binding Proteins; D011956:Receptors, Cell Surface / Q000378:metabolism*; D011973:Receptors, LDL / Q000378:metabolism; D018110:Receptors, Lipoprotein
D002352:Carrier Proteins; D008075:Lipoproteins, HDL; D026503:Low Density Lipoprotein Receptor-Related Protein-1; D016601:RNA-Binding Proteins; D011956:Receptors, Cell Surface; D011973:Receptors, LDL; D018110:Receptors, Lipoprotein; C036053:VLDL receptor; C031616:high density lipoprotein receptors; C075197:high density lipoprotein binding protein; D002784:Cholesterol