Role of Mitochondria in Nonalcoholic Fatty Liver Disease

International Journal of Molecular Sciences

Fatiha Nassir¹ 

[1] Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Missouri, Columbia, MO 65212, USA; E-Mail

关键词: NAFLD;    NASH;    mitochondria;    liver;    steatosis;    fatty acid oxidation;    PGC-1α;    sirtuin-1 (SIRT1);    sirtuin-3 (SIRT3);   

DOI  :  10.3390/ijms15058713

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland