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. 2020 Nov 7;26(41):6304–6321. doi: 10.3748/wjg.v26.i41.6304

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©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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/

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Hepatic fibrosis and subsequent cirrhosis caused by a variety of different etiologies, is a balance between fibrosis formation (fibrogenesis) and fibrinolysis. Anti-fibrotic drugs target a variety of mechanisms involved in this balance between formation of extracellular matrix and subsequent fibrosis and its breakdown (fibrinolysis). Transforming growth factor-β is the most influential cytokine in the induction of fibrogenesis, as it plays a pivotal role in hepatic stellate cells activation and myofibroblast formation. NAFLD: Nonalcoholic fatty liver disease; NASH: Nonalcoholic steatohepatitis; MAFLD: Metabolic associated fatty liver disease; HSC: Hepatic stellate cells; ECM: Extracellular matrix.