Role of mitochondria in nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) affects about 30% of the general population in the United States and includes a spectrum of disease that includes simple steatosis, non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis. Significant insight has been gained into our understanding of the...

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Bibliographic Details
Published in:International journal of molecular sciences Vol. 15; no. 5; pp. 8713 - 8742
Main Authors: Nassir, Fatiha, Ibdah, Jamal A
Format: Journal Article
Language:English
Published: Switzerland MDPI AG 15-05-2014
Molecular Diversity Preservation International (MDPI)
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Summary:Nonalcoholic fatty liver disease (NAFLD) affects about 30% of the general population in the United States and includes a spectrum of disease that includes simple steatosis, non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis. Significant insight has been gained into our understanding of the pathogenesis of NALFD; however the key metabolic aberrations underlying lipid accumulation in hepatocytes and the progression of NAFLD remain to be elucidated. Accumulating and emerging evidence indicate that hepatic mitochondria play a critical role in the development and pathogenesis of steatosis and NAFLD. Here, we review studies that document a link between the pathogenesis of NAFLD and hepatic mitochondrial dysfunction with particular focus on new insights into the role of impaired fatty acid oxidation, the transcription factor peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), and sirtuins in development and progression of NAFLD.
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ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms15058713