Cellular mechanisms of cholestasis.
Concepts regarding the pathogenesis of cholestasis continue to evolve as investigational techniques improve and molecular mechanisms of bile formation are clarified. With the accumulation of information it is becoming increasingly evident that cholestasis results from not one but multiple disturbances in the sequence of events responsible for bile production. In addition to the inhibition of bile flow attributable to initiating events, cholestasis itself may inhibit bile flow by altering the intra- and extracellular environments of liver cells. Many questions about cholestasis remain unanswered, but future directions for research are suggested by the information currently available.
D008841:Actin Cytoskeleton / Q000378:metabolism; D000818:Animals; D001646:Bile / Q000378:metabolism* / Q000502:physiology; D001647:Bile Acids and Salts / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism; D002118:Calcium / Q000097:blood / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D002780:Cholestasis, Intrahepatic / Q000139:chemically induced / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D064420:Drug-Related Side Effects and Adverse Reactions; D004847:Epithelial Cells; D004848:Epithelium / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism; D006801:Humans; D008099:Liver / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D008862:Microsomes, Liver / Q000378:metabolism; D051381:Rats; D012106:Research; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000378:metabolism; D013577:Syndrome
D001647:Bile Acids and Salts; D000254:Sodium-Potassium-Exchanging ATPase; D002118:Calcium