Liver fibrogenesis in non-alcoholic steatohepatitis

被引:31
作者
Bian, Zhaolian [1 ,2 ]
Ma, Xiong [1 ,2 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Shanghai Inst Digest & Dis,Div Gastroenterol & He, Shanghai 200001, Peoples R China
[2] Shanghai Jiao Tong Univ, Minist Hlth, Key Lab Gastroenterol & Hepatol, Shanghai 200001, Peoples R China
来源
FRONTIERS IN PHYSIOLOGY | 2012年 / 3卷
关键词
non-alcoholic fatty liver disease; hepatic stellate cell; hepatic fibrosis; cirrhosis; HEPATIC STELLATE CELLS; KILLER T-CELLS; MORBIDLY OBESE-PATIENTS; PLACEBO-CONTROLLED TRIAL; FATTY LIVER; INSULIN-RESISTANCE; OXIDATIVE STRESS; LIPID-PEROXIDATION; RAT MODEL; FIBROSIS;
D O I
10.3389/fphys.2012.00248
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Non-alcoholic fatty liver disease (NAFLD) is emerging as one of the most common chronic liver diseases in developed western countries. Non-alcoholic steatohepatitis (NASH) is the most severe form of NAFLD, and can progress to more severe forms of liver disease, including fibrosis, cirrhosis, and even hepatocellular carcinoma. The activation of hepatic stellate cells plays a critical role in NASH-related fibrogenesis. Multiple factors, such as insulin resistance, oxidative stress, pro-inflammatory cytokines and adipokines, and innate immune responses, are known to contribute to the development of NASH-related fibrogenesis. Furthermore, these factors may share synergistic interactions, which could contribute to the process of liver fibrosis. Given the complex etiology of NASH, combined treatment regimes that target these different factors provide potential treatment strategies for NASH-related liver fibrosis.
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页数:7
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