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Mitochondrial Dysfunction in the Transition from NASH to HCC

1
Institut de Recherches Cliniques de Montréal (IRCM), Montreal, Quebec, QC H2W 1R7, Canada
2
Faculty of Medicine, University of Montreal, Montreal, Quebec, QC H3G 2M1, Canada
3
Division of Experimental Medicine, McGill University, Montreal, Quebec, QC H4A 3J1, Canada
*
Author to whom correspondence should be addressed.
Metabolites 2019, 9(10), 233; https://doi.org/10.3390/metabo9100233
Received: 27 August 2019 / Revised: 26 September 2019 / Accepted: 11 October 2019 / Published: 16 October 2019
(This article belongs to the Special Issue Mitochondria and Metabolism in Disorders)
The liver constantly adapts to meet energy requirements of the whole body. Despite its remarkable adaptative capacity, prolonged exposure of liver cells to harmful environmental cues (such as diets rich in fat, sugar, and cholesterol) results in the development of chronic liver diseases (including non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH)) that can progress to hepatocellular carcinoma (HCC). The pathogenesis of these diseases is extremely complex, multifactorial, and poorly understood. Emerging evidence suggests that mitochondrial dysfunction or maladaptation contributes to detrimental effects on hepatocyte bioenergetics, reactive oxygen species (ROS) homeostasis, endoplasmic reticulum (ER) stress, inflammation, and cell death leading to NASH and HCC. The present review highlights the potential contribution of altered mitochondria function to NASH-related HCC and discusses how agents targeting this organelle could provide interesting treatment strategies for these diseases. View Full-Text
Keywords: mitochondria; metabolism; liver; NAFLD; NASH; HCC mitochondria; metabolism; liver; NAFLD; NASH; HCC
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Léveillé, M.; Estall, J.L. Mitochondrial Dysfunction in the Transition from NASH to HCC. Metabolites 2019, 9, 233.

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