| Autor: |
Cazanave SC; Department of Internal Medicine, Division of Gastroenterology, Hepatology and Nutrition; Virginia Commonwealth University School of Medicine ; Richmond, VA USA., Sanyal AJ; Department of Internal Medicine, Division of Gastroenterology, Hepatology and Nutrition; Virginia Commonwealth University School of Medicine ; Richmond, VA USA. |
| Jazyk: |
angličtina |
| Zdroj: |
Molecular & cellular oncology [Mol Cell Oncol] 2014 Oct 29; Vol. 2 (2), pp. e968065. Date of Electronic Publication: 2014 Oct 29 (Print Publication: 2015). |
| DOI: |
10.4161/23723548.2014.968065 |
| Abstrakt: |
Hepatocyte apoptosis in association with oxidative stress represent key pathogenic factors involved in tumor development in patients with non-alcoholic fatty liver disease (NAFLD). In our recent study, we established that cellular degradation of Kelch-like ECH-associated protein 1 (KEAP1) through sequestrosome (SQSTM)1/p62-dependent autophagy activates c-Jun NH2 terminal kinase (JNK), upregulates expression of Bcl-2-interacting mediator (BIM) and p53 upregulated modulator of apoptosis (PUMA), and contributes to hepatocyte apoptosis induced by saturated free fatty acids. These findings raise the possibility that dysregulation of KEAP1 may contribute to liver cell death and tumorigenesis during chronic inflammatory liver disease. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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