The Progression of Liver Fibrosis in Non-alcoholic Fatty Liver Disease.
10.4166/kjg.2017.69.6.341
- Author:
Moon Young KIM
1
Author Information
1. Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea. drkimmy@yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
Non-alcoholic fatty liver disease;
Fibrosis;
Inflammation;
Insulin resistance
- MeSH:
Aging;
Apoptosis;
Disease Progression;
Fatty Acids, Nonesterified;
Fatty Liver;
Fibrosis;
Hepatocytes;
Inflammasomes;
Inflammation;
Insulin Resistance;
Liver Cirrhosis*;
Liver*;
Non-alcoholic Fatty Liver Disease*;
Obesity;
Oxidative Stress;
Stem Cells
- From:The Korean Journal of Gastroenterology
2017;69(6):341-347
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Understanding the pathogenesis of non-alcoholic steatohepatitis (NASH) and its fibrosis progression is still evolving. Nonetheless, current evidence suggests that mechanisms involved are very complex parallel processes with multiple metabolic factors. Lipotoxicity related with excess saturated free fatty acids, obesity, and insulin resistance acts as the central driver of cellular injury via oxidative stress. Hepatocyte apoptosis and/or senescence are also contribute to the activation of inflammasome via various intra- and inter-cellular signaling mechanisms that lead to fibrosis. Current evidence suggests that periportal components, including ductular reaction and expansion of the hepatic progenitor cell compartment, may be involved and that the T-helper 17 cell response may mediate disease progression. This review aims to provide a brief overview of the pathogenesis of NASH and fibrosis progression from inflammation to fibrosis.
