Molecular alterations in hepatocyte transport mechanisms in acquired cholestatic liver disorders.
Recent advances in the molecular cloning of membrane transport systems that determine bile formation have facilitated studies of the molecular mechanisms of cholestatic liver disease. The present review summarizes what has been learned about the molecular alterations of these membrane transporters in hepatocytes and cholangiocytes in acquired cholestatic liver disorders. Much of this information has been obtained from the study of animal models of cholestasis and from more limited studies in clinical cholestatic liver diseases. Many of these responses may be interpreted as adaptations that serve to diminish cholestatic liver injury.
Lee
J
J
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8019, USA.
Boyer
J L
JL
D000074020:ATP Binding Cassette Transporter, Subfamily B, Member 11; D018528:ATP-Binding Cassette Transporters / Q000235:genetics; D000818:Animals; D001646:Bile / Q000502:physiology; D001659:Biliary Tract / Q000166:cytology / Q000378:metabolism; D001693:Biological Transport, Active; D002779:Cholestasis / Q000209:etiology / Q000235:genetics / Q000378:metabolism*; D022781:Hepatocytes / Q000378:metabolism*; D006801:Humans; D008115:Liver Regeneration
C093491:ABCB11 protein, human; D000074020:ATP Binding Cassette Transporter, Subfamily B, Member 11; D018528:ATP-Binding Cassette Transporters