Ethanol and hepatocellular injury.
Hepatocellular injury that results from chronic alcohol abuse may be a consequence of (1) augmented viremia in hepatitis C virus; (2) the carcinogenic effect of DNA, which results from the combination of alcohol-induced CYP2E1 and ingestion of low levels of carcinogenic compounds or choline deficiency; (3) differential proliferation of hepatocytes versus nonparenchymal cells during injury, regeneration, and repair; (4) alteration of the regenerative response of hepatocytes in response to agonists, which stimulate the cell cycle through membrane signal transduction-nuclear pathways; (5) Kupffer cell activation by endotoxin, which generates cytokines that signal hepatocellular programmed cell death (apoptosis) through signal transduction mechanisms; or (6) dietary and immune mechanisms (i.e., formation of neoantigens).
French
S W
SW
Division of Anatomic Pathology, Harbor-UCLA Medical Center, Torrance, USA.
D000437:Alcoholism / Q000473:pathology / Q000821:virology*; D016207:Cytokines; D006509:Hepatitis B / Q000473:pathology; D006526:Hepatitis C / Q000473:pathology; D006801:Humans; D008099:Liver / Q000473:pathology / Q000821:virology; D008108:Liver Diseases, Alcoholic / Q000473:pathology / Q000503:physiopathology / Q000821:virology*; D008115:Liver Regeneration; D009336:Necrosis; D015398:Signal Transduction
D016207:Cytokines