Molecular Pathogenesis of NASH

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 fr...

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Main Authors: Alessandra Caligiuri, Alessandra Gentilini, Fabio Marra
Format: Article
Language:English
Published: MDPI AG 2016-09-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:http://www.mdpi.com/1422-0067/17/9/1575
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spelling doaj-1793b9788ba94af1b5a433942f4eb69e2020-11-24T22:22:24ZengMDPI AGInternational Journal of Molecular Sciences1422-00672016-09-01179157510.3390/ijms17091575ijms17091575Molecular Pathogenesis of NASHAlessandra Caligiuri0Alessandra Gentilini1Fabio Marra2Dipartimento di Medicina Sperimentale e Clinica, Università degli Studi di Firenze, Firenze 50121, ItalyDipartimento di Medicina Sperimentale e Clinica, Università degli Studi di Firenze, Firenze 50121, ItalyDipartimento di Medicina Sperimentale e Clinica, Università degli Studi di Firenze, Firenze 50121, ItalyNonalcoholic 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.http://www.mdpi.com/1422-0067/17/9/1575fibrosisinflammationchemokinesgeneticsmicrobiotapattern-recognition receptorsnuclear receptorshepatic stellate cellsmacrophages
collection DOAJ
language English
format Article
sources DOAJ
author Alessandra Caligiuri
Alessandra Gentilini
Fabio Marra
spellingShingle Alessandra Caligiuri
Alessandra Gentilini
Fabio Marra
Molecular Pathogenesis of NASH
International Journal of Molecular Sciences
fibrosis
inflammation
chemokines
genetics
microbiota
pattern-recognition receptors
nuclear receptors
hepatic stellate cells
macrophages
author_facet Alessandra Caligiuri
Alessandra Gentilini
Fabio Marra
author_sort Alessandra Caligiuri
title Molecular Pathogenesis of NASH
title_short Molecular Pathogenesis of NASH
title_full Molecular Pathogenesis of NASH
title_fullStr Molecular Pathogenesis of NASH
title_full_unstemmed Molecular Pathogenesis of NASH
title_sort molecular pathogenesis of nash
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1422-0067
publishDate 2016-09-01
description 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.
topic fibrosis
inflammation
chemokines
genetics
microbiota
pattern-recognition receptors
nuclear receptors
hepatic stellate cells
macrophages
url http://www.mdpi.com/1422-0067/17/9/1575
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