期刊
TOXICOLOGICAL SCIENCES
卷 150, 期 2, 页码 261-268出版社
OXFORD UNIV PRESS
DOI: 10.1093/toxsci/kfw018
关键词
non-alcoholic fatty liver disease; steatosis; adverse outcome pathway; mechanistic toxicology; high-throughput screening assays; chemical risk assessment
类别
资金
- U.S. Environmental Protection Agency Office of Research and Development
Hepatic steatosis is a condition were fat accumulates in the liver and it is associated with extra-hepatic diseases related to metabolic syndrome and systemic energy metabolism. If not reversed, steatosis can progress to steatohepatitis and irreversible stages of liver disease including fibrosis, cirrhosis, hepatocellular carcinoma, and death. From a public health standpoint, identifying chemical exposures that may be factors in steatosis etiology are important for preventing hepatotoxicity and liver disease progression. It is therefore important to identify the biological events that are key for steatosis pathology mediated by chemical exposure. In this review, we give a current overview of the complex biological cascades that can disrupt lipid homeostasis in hepatocytes in the context of 4 apical key events central to hepatic lipid retention: hepatic fatty acid (FA) uptake, de novo FA and lipid synthesis, FA oxidation, and lipid efflux. Our goal is to review these key cellular events and visually summarize them using a network for application in pathway-based toxicity testing. This effort provides a foundation to improve next-generation chemical screening efforts that may be used to prevent and ultimately reverse the growing incidence of fatty liver disease in our population.
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