Alcohol and liver fibrosis.
Alcoholic liver disease involves significant crosstalk among intracellular signaling events in the liver. Overall, inflammatory and innate immune responses in Kupffer cells due to elevated gut-derived plasma endotoxin levels, increased reactive oxygen species-induced damage, and profibrogenic factors such as acetaldehyde or lipid peroxidation products contribute to activation of hepatic stellate cells, the key cell type involved in liver fibrosis. Using in vitro and in vivo approaches, there has been great progress in our understanding of the mechanisms leading to liver fibrosis: potential biomarkers of fibrosis have been identified, and several candidate targets for antifibrotic drugs have been elucidated.
Cubero
Francisco Javier
FJ
Department of Medicine, Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029, USA.
Urtasun
Raquel
R
Nieto
Natalia
N
D000428:Alcohol Drinking / Q000009:adverse effects*; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D018450:Disease Progression; D000431:Ethanol / Q000378:metabolism / Q000633:toxicity*; D005109:Extracellular Matrix / Q000378:metabolism; D055166:Hepatic Stellate Cells / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D015227:Lipid Peroxidation; D008099:Liver / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D008104:Liver Cirrhosis, Alcoholic / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism; D008106:Liver Cirrhosis, Experimental; D018384:Oxidative Stress; D012307:Risk Factors
D015415:Biomarkers; D018836:Inflammation Mediators; D000431:Ethanol