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. 2016 Oct 8;8(28):1157–1168. doi: 10.4254/wjh.v8.i28.1157

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©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.

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.

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Development of fibrosis and cirrhosis in autoimmune liver disease. Persistent autoimmune-mediated inflammation and liver cell injury leads to the activation and differentiation of quiescent hepatic stellate cells (HSC) and portal fibroblasts (PF) into activated myofibroblasts. These proliferative, pro-inflammatory and pro-fibrogenic myofibroblasts increase collagen synthesis and deposit extracellular matrix proteins (ECM), leading to the development of fibrous scar tissue. Cirrhosis, characterised by significant fibrosis and nodular regeneration, eventually ensues, with the resultant loss of liver function and eventually liver failure.