Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma

被引:11
作者
Sasaki-Tanaka, Reina [1 ]
Ray, Ranjit [2 ,3 ]
Moriyama, Mitsuhiko [1 ]
Ray, Ratna B. [4 ]
Kanda, Tatsuo [1 ]
机构
[1] Nihon Univ, Dept Med, Div Gastroenterol & Hepatol, Sch Med,Itabashi Ku, 30-1 Oyaguchi Kamicho, Tokyo 1738610, Japan
[2] St Louis Univ, Dept Internal Med, St Louis, MO 63104 USA
[3] St Louis Univ, Dept Mol Microbiol & Immunol, St Louis, MO 63104 USA
[4] St Louis Univ, Dept Pathol, St Louis, MO 63104 USA
基金
美国国家卫生研究院;
关键词
hepatocellular carcinoma; alcohol; acetaldehyde; ALDH; cirrhosis; ACTIVATED PROTEIN-KINASE; GENOME-WIDE ASSOCIATION; INDUCED LIVER-INJURY; FATTY LIVER; GENETIC POLYMORPHISMS; COMPLEMENT-SYSTEM; RISK LOCI; ETHANOL; CANCER; HEPATITIS;
D O I
10.3390/ijms23179679
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alcohol is the one of the major causes of liver diseases and promotes liver cirrhosis and hepatocellular carcinoma (HCC). In hepatocytes, alcohol is converted to acetaldehyde, which causes hepatic steatosis, cellular apoptosis, endoplasmic reticulum stress, peroxidation, production of cytokines and reduces immune surveillance. Endotoxin and lipopolysaccharide produced from intestinal bacteria also enhance the production of cytokines. The development of hepatic fibrosis and the occurrence of HCC are induced by these alcohol metabolites. Several host genetic factors have recently been identified in this process. Here, we reviewed the molecular mechanism associated with HCC in alcoholic liver disease.
引用
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页数:12
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