alexa Role of ER Stress in Inflammasome Activation and Non-Alcoholic Fatty Liver Disease Progression
ISSN: 2168-9431

Single Cell Biology
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Commentary

Role of ER Stress in Inflammasome Activation and Non-Alcoholic Fatty Liver Disease Progression

Cynthia Lebeaupin1,2, Deborah Vallee1,2, Philippe Gual1,2 and Beatrice Bailly-Maitre1,2,*

1INSERM, U1065, Equipe 8 “Complications hépatiques de l’obésité”, Bâtiment Universitaire ARCHIMED Nice, France

2Université de Nice Sophia Antipolis, Nice, France

Corresponding Author:
Bailly-Maitre Beatrice
Batiment Universitaire ARCHIMED, INSERM, U1065
Team 8 “Hepatic complications in obesity”, 151 route Saint
Antoine de Ginestière, BP 2 3194, 06204 Nice Cedex 03, France
Tel: +33(0)489064238
Fax: +33(0)489064221
E-mail: [email protected]

Received date: May 16, 2016; Accepted date: May 30, 2016; Published date: Jun 01, 2016

Citation: Lebeaupin C, Vallee D, Gual P, Bailly-Maitre B (2016) Role of ER Stress in Inflammasome Activation and Non-Alcoholic Fatty Liver Disease Progression . Single Cell Biol 5:140. doi:10.4172/2168- 9431.1000140

Copyright: © 2016 Lebeaupin C, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

With the prevalence of obesity increasing worldwide, nonalcoholic fatty liver disease (NAFLD) has become the most common form of chronic liver disease. Despite this, knowledge about the molecular mechanisms involved in NAFLD progression is still limited. Recent findings have shown that endoplasmic reticulum (ER) stress links inflammation and hepatocyte death, inherent to the transition from simple steatosis to nonalcoholic steatohepatitis (NASH). Here, we emphasize the central role of the ER stress response and its crosstalk with the inflammasome. We hope to provide new insight on the identification of ER stress-dependent pathways that contribute substantially to chronic liver disease progression as important triggers of cell death and inflammation, and therefore may represent potential therapeutic strategies.

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