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Review
. 2016 May;73(10):1969-87.
doi: 10.1007/s00018-016-2161-x. Epub 2016 Feb 19.

Pathogenesis of nonalcoholic steatohepatitis

Wensheng Liu  1 , Robert D Baker  2 , Tavleen Bhatia  2 , Lixin Zhu  2 , Susan S Baker  3
Affiliations
Review

Pathogenesis of nonalcoholic steatohepatitis

Wensheng Liu et al. Cell Mol Life Sci. 2016 May.

Abstract

Nonalcoholic steatohepatitis (NASH) is a severe form of nonalcoholic fatty liver disease and a risk factor for cirrhosis and hepatocellular carcinoma. The pathological features of NASH include steatosis, hepatocyte injury, inflammation, and various degrees of fibrosis. Steatosis reflects disordered lipid metabolism. Insulin resistance and excessive fatty acid influx to the liver are two important contributing factors. Steatosis is also likely associated with lipotoxicity and cellular stresses such as oxidative stress and endoplasmic reticulum stress, which result in hepatocyte injury. Inflammation and fibrosis are frequently triggered by various signals such as proinflammatory cytokines and chemokines, released by injuried hepatocytes and activated Kupffer cells. Although much progress has been made, the pathogenesis of NASH is not fully elucidated. The purpose of this review is to discuss the current understanding of NASH pathogenesis, mainly focusing on factors contributing to steatosis, hepatocyte injury, inflammation, and fibrosis.

Keywords: Apoptosis; Autophagy; Genetic predisposition; Gut microbiota; Hepatic stellate cells.

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Figures

Fig. 1
Fig. 1
Factors contributing to hepatic steatosis. +: promoting steatosis; −: reducing steatosis
Fig. 2
Fig. 2
Hepatocyte injury and apoptosis in NAFLD
Fig. 3
Fig. 3
Inflammation in NASH
Fig. 4
Fig. 4
Fibrosis in NASH
See this image and copyright information in PMC

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