Combined alcoholic and non-alcoholic steatohepatitis.

ACC, acetyl-CoA carboxylase ALD ALD, alcohol-related liver disease ASH ASH, alcohol-related steatohepatitis ASK-1, apoptosis signal-regulating kinase 1 Alcohol BMI, body mass index CLD, chronic liver disease CPT, carnitine palmitoyltransferase DNL, de novo lipogenesis EASL, European Association for the Study of the Liver ER, endoplasmic reticulum FXR, farnesoid X receptor HCC, hepatocellular carcinoma HSD17B13, hydroxysteroid 17-beta dehydrogenase 13 IL, interleukin LPS, lipopolysaccharide MBOAT7, membrane bound O-acyl transferase 7 MELD, model for end-stage liver disease NAFLD NAFLD, non-alcoholic fatty liver disease NASH NASH, non-alcoholic steatohepatitis OR, odds ratio PAMP, pathogen-associated molecular pattern PI3K, phosphatidylinositol-3-kinase PIP3, phosphatidylinositol 3,4,5-triphosphate PNPLA3, palatin-like phospholipase domain-containing 3 PRKCE, protein kinase C Epsilon ROS, reactive oxygen species SREBP-1c, sterol regulatory element binding protein-1c TLR, Toll-like receptor TM6SF2, transmembrane 6 superfamily member 2 TNF-α, tumour necrosis factor-α WHO, World Health Organization diabetes metabolic syndrome obesity

Journal

JHEP reports : innovation in hepatology
ISSN: 2589-5559
Titre abrégé: JHEP Rep
Pays: Netherlands
ID NLM: 101761237

Informations de publication

Date de publication:
Jun 2020
Historique:
received: 04 12 2019
revised: 18 02 2020
accepted: 10 03 2020
entrez: 10 6 2020
pubmed: 10 6 2020
medline: 10 6 2020
Statut: epublish

Résumé

While metabolic syndrome and alcohol consumption are the two main causes of chronic liver disease, one of the two conditions is often predominant, with the other acting as a cofactor of morbimortality. It has been shown that obesity and alcohol act synergistically to increase the risk of fibrosis progression, hepatic carcinogenesis and mortality, while genetic polymorphisms can strongly influence disease progression. Based on common pathogenic pathways, there are several potential targets that could be used to treat both diseases; based on the prevalence and incidence of these diseases, new therapies and clinical trials are needed urgently.

Identifiants

pubmed: 32514497
doi: 10.1016/j.jhepr.2020.100101
pii: S2589-5559(20)30035-5
pii: 100101
pmc: PMC7267467
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

100101

Informations de copyright

© 2020 The Authors.

Déclaration de conflit d'intérêts

The authors declare no conflicts of interest that pertain to this work. Please refer to the accompanying ICMJE disclosure forms for further details.

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Auteurs

Line Carolle Ntandja Wandji (LC)

Service des maladies de l'appareil digestif, Hôpital Huriez, Rue Polonowski, 59037 Lille Cedex, France.
Université Lille Nord de France, Lille, France.
Unité INSERM 995, Lille, France.

Viviane Gnemmi (V)

Centre de Biologie-Pathologie, Lille, France.

Philippe Mathurin (P)

Service des maladies de l'appareil digestif, Hôpital Huriez, Rue Polonowski, 59037 Lille Cedex, France.
Université Lille Nord de France, Lille, France.
Unité INSERM 995, Lille, France.

Alexandre Louvet (A)

Service des maladies de l'appareil digestif, Hôpital Huriez, Rue Polonowski, 59037 Lille Cedex, France.
Université Lille Nord de France, Lille, France.
Unité INSERM 995, Lille, France.

Classifications MeSH