Novel Molecular Mechanisms in the Development of Non-Alcoholic Steatohepatitis.
- Author:
Davide POVERO
1
;
Ariel E FELDSTEIN
Author Information
- Publication Type:Review
- Keywords: Angiogenesis; Cell death; Cirrhosis; Extracellular vesicles; Lipotoxicity
- MeSH: Adult; Cell Death; Child; Diagnosis; Fatty Liver*; Fibrosis; Genetics; Hepatocytes; Humans; Inflammation; Liver; Liver Cirrhosis; Liver Diseases; Microbiota; Neovascularization, Pathologic
- From:Diabetes & Metabolism Journal 2016;40(1):1-11
- CountryRepublic of Korea
- Language:English
- Abstract: Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease in adults and children worldwide. NAFLD has become a severe health issue and it can progress towards a more severe form of the disease, the non-alcoholic steatohepatitis (NASH). A combination of environmental factors, host genetics, and gut microbiota leads to excessive accumulation of lipids in the liver (steatosis), which may result in lipotoxicity and trigger hepatocyte cell death, liver inflammation, fibrosis, and pathological angiogenesis. NASH can further progress towards liver cirrhosis and cancer. Over the last few years, cell-derived extracellular vesicles (EVs) have been identified as effective cell-to-cell messengers that transfer several bioactive molecules in target cells, modulating the pathogenesis and progression of NASH. In this review, we focused on recently highlighted aspects of molecular pathogenesis of NASH, mediated by EVs via their bioactive components. The studies included in this review summarize the state of art regarding the role of EVs during the progression of NASH and bring novel insight about the potential use of EVs for diagnosis and therapeutic strategies for patients with this disease.
