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Int. J. Mol. Sci. 2016, 17(9), 1575; doi:10.3390/ijms17091575

Molecular Pathogenesis of NASH

Dipartimento di Medicina Sperimentale e Clinica, Università degli Studi di Firenze, Firenze 50121, Italy
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Academic Editors: Giovanni Targher and Amedeo Lonardo
Received: 14 July 2016 / Revised: 5 September 2016 / Accepted: 7 September 2016 / Published: 20 September 2016
(This article belongs to the Special Issue Non-Alcoholic Fatty Liver Disease Research 2016)
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Abstract

Nonalcoholic steatohepatitis (NASH) is the main cause of chronic liver disease in the Western world and a major health problem, owing to its close association with obesity, diabetes, and the metabolic syndrome. NASH progression results from numerous events originating within the liver, as well as from signals derived from the adipose tissue and the gastrointestinal tract. In a fraction of NASH patients, disease may progress, eventually leading to advanced fibrosis, cirrhosis and hepatocellular carcinoma. Understanding the mechanisms leading to NASH and its evolution to cirrhosis is critical to identifying effective approaches for the treatment of this condition. In this review, we focus on some of the most recent data reported on the pathogenesis of NASH and its fibrogenic progression, highlighting potential targets for treatment or identification of biomarkers of disease progression. View Full-Text
Keywords: fibrosis; inflammation; chemokines; genetics; microbiota; pattern-recognition receptors; nuclear receptors; hepatic stellate cells; macrophages fibrosis; inflammation; chemokines; genetics; microbiota; pattern-recognition receptors; nuclear receptors; hepatic stellate cells; macrophages
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Caligiuri, A.; Gentilini, A.; Marra, F. Molecular Pathogenesis of NASH. Int. J. Mol. Sci. 2016, 17, 1575.

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