4.3 Review

Alcohol and Liver Fibrosis

期刊

SEMINARS IN LIVER DISEASE
卷 29, 期 2, 页码 211-221

出版社

THIEME MEDICAL PUBL INC
DOI: 10.1055/s-0029-1214376

关键词

Kupffer cells; hepatic stellate cells; alcohol; extracellular matrix protein; fibrosis

资金

  1. US Public Health Service [1RO1 DK 06928]
  2. National Institute of Diabetes and Digestive and Kidney Diseases
  3. National Institute on Alcohol Abuse and Alcoholism [1R01 AA017733, IP20AA017067]
  4. New York Center for Systems Biology, (NYCSB)
  5. Government of Navarre (Spain)
  6. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK069286] Funding Source: NIH RePORTER
  7. NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [P20AA017067, R01AA017733] Funding Source: NIH RePORTER

向作者/读者索取更多资源

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.

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