Del Campo JA, Gallego P, Grande L. Role of inflammatory response in liver diseases: Therapeutic strategies. World J Hepatol 2018; 10(1): 1-7 [PMID: 29399273 DOI: 10.4254/wjh.v10.i1.1]
Corresponding Author of This Article
José A Del Campo, PhD, Department of Digestive Diseases, Valme University Hospital and CIBERehd, Avda. Bellavista s/n, Sevilla 41014, Spain. jantonio.delcampo@ciberehd.org
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Hepatol. Jan 27, 2018; 10(1): 1-7 Published online Jan 27, 2018. doi: 10.4254/wjh.v10.i1.1
Role of inflammatory response in liver diseases: Therapeutic strategies
José A Del Campo, Paloma Gallego, Lourdes Grande
José A Del Campo, Paloma Gallego, Lourdes Grande, Department of Digestive Diseases, Valme University Hospital and CIBERehd, Sevilla 41014, Spain
Author contributions: Del Campo JA designed the study and drafted the manuscript; Gallego P and Grande L drafted the manuscript and designed the figure.
Supported by Andalusian Government, No. PI0892-2012; Instituto de Salud Carlos III, PI14/01349 co-financed by the European Regional Development Fund (ERDF); JA Del Campo supported by Nicolás Monardes Program from Servicio Andaluz de Salud (SAS).
Conflict-of-interest statement: Authors declare no conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: José A Del Campo, PhD, Department of Digestive Diseases, Valme University Hospital and CIBERehd, Avda. Bellavista s/n, Sevilla 41014, Spain. jantonio.delcampo@ciberehd.org
Telephone: +34-955-015485 Fax: +34-955-015485
Received: November 8, 2017 Peer-review started: November 9, 2017 First decision: December 4, 2017 Revised: December 21, 2017 Accepted: January 15, 2018 Article in press: January 15, 2018 Published online: January 27, 2018 Processing time: 77 Days and 21.9 Hours
Core Tip
Core tip: Inflammasomes are newly recognized vital players in innate immunity. Several factors have been identified able to activate the NLRP3 inflammasome. Inappropriate activation of NLRP3 can contribute to the onset and progression of various diseases, particularly age-related diseases. It is well established that hepatitis C virus infection plays a critical role in the promotion of liver inflammation and disease, inducing the production of IL-1β and the activation of NLRP3. NLRP3 inflammasome gain of function aggravates liver disease, resulting in severe liver fibrosis and lately, hepatocellular carcinoma. In non-alcoholic fatty liver disease, the regulation of inflammation processes may prevent the progression of non-alcoholic steatohepatitis to fibrosis.
