Abstract
Purpose of Review
About 15–25% of patients with simple steatosis of nonalcoholic fatty liver disease progresses to nonalcoholic steatohepatitis (NASH), and the underlying mechanism for this progression has not been elucidated. NASH ultimately could progress to cirrhosis, an irreversible condition.
Recent Findings
Farnesoid X receptor (FXR) has been studied for its role in modulating inflammation, and the expression of FXR is down-regulated during NASH development. FXR deficiency has shown to progress and exacerbate NASH development, and FXR activation has been protective against liver inflammation associated with NASH. The expression of factors in both the adaptive and innate immune response in the liver are regulated in a FXR-dependent and -independent manner.
Summary
Therefore, understanding key signaling pathways of liver inflammation in NASH is important to determine essential components that predispose, progress, or exacerbate NASH. FXR has been identified as a therapeutic target for NASH to prevent liver inflammation.
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Acknowledgements
The authors would like to acknowledge the NIH Grant, GM104037, to support Dr. Grace L. Guo’s research and the NIH/NIEHS Training Grant, T32ES007148, to support Dr. Laura E. Armstrong’s post-doctoral training.
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Laura E. Armstrong and Grace L. Guo declare that they have no conflict of interest.
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This article is part of the Topical Collection on Liver & Xenobiotic Metabolism
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Armstrong, L.E., Guo, G.L. Role of FXR in Liver Inflammation During Nonalcoholic Steatohepatitis. Curr Pharmacol Rep 3, 92–100 (2017). https://doi.org/10.1007/s40495-017-0085-2
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DOI: https://doi.org/10.1007/s40495-017-0085-2