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World J Gastrointest Pharmacol Ther. Nov 5, 2024; 15(6): 97381
Published online Nov 5, 2024. doi: 10.4292/wjgpt.v15.i6.97381
Regression of hepatic fibrosis after pharmacological therapy for nonalcoholic steatohepatitis
Mohamed Abdel-Samiee, Essam Salah Ibrahim, Mohamed Kohla, Eman Abdelsameea, Mohsen Salama
Mohamed Abdel-Samiee, Mohamed Kohla, Eman Abdelsameea, Mohsen Salama, Department of Hepatology and Gastroenterology, National Liver Institute, Menoufia University, Shebin El-Kom 32511, Egypt
Essam Salah Ibrahim, Department of Medicine, RCSI Medical University of Bahrain, Adliya 15503, Bahrain
Author contributions: Abdelsameea E designed the research; Abdel-Samiee M, Ibrahim ES, Kohla M, Abdelsameea E, and Salama M analyzed data; Abdel-Samiee M, Ibrahim ES, Kohla M, Abdelsameea E, Salama M contributed to writing the paper, drafting, and revising critically; Abdel-Samiee M, Ibrahim ES, Kohla M, Abdelsameea E, Salama M approved the final version of the manuscript for submission.
Conflict-of-interest statement: All authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Open-Access: 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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Eman Abdelsameea, MD, Full Professor, Department of Hepatology and Gastroenterology, National Liver Institute, Menoufia University, National Liver Institute, Menoufia University, Shebin El-Kom 32511, Egypt. eabdelsameea@liver-eg.org
Received: May 29, 2024
Revised: August 28, 2024
Accepted: September 23, 2024
Published online: November 5, 2024
Processing time: 148 Days and 5.3 Hours
Abstract

The global incidence of nonalcoholic fatty liver disease (NAFLD) is escalating considerably. NAFLD covers a range of liver conditions from simple steatosis to the more severe form known as nonalcoholic steatohepatitis, which involves chronic liver inflammation and the transformation of hepatic stellate cells into myofibroblasts that generate excess extracellular matrix, leading to fibrosis. Hepatocyte ballooning is a key catalyst for fibrosis progression, potentially advancing to cirrhosis and its decompensated state. Fibrosis is a critical prognostic factor for outcomes in patients with NAFLD; therefore, those with substantial fibrosis require timely intervention. Although liver biopsy is the most reliable method for fibrosis detection, it is associated with certain risks and limitations, particularly in routine screening. Consequently, various noninvasive diagnostic techniques have been introduced. This review examines the increasing prevalence of NAFLD, evaluates the noninvasive diagnostic techniques for fibrosis, and assesses their efficacy in staging the disease. In addition, it critically appraises current and emerging antifibrotic therapies, focusing on their mechanisms, efficacy, and potential in reversing fibrosis. This review underscores the urgent need for effective therapeutic strategies, given the dire consequences of advanced fibrosis.

Keywords: Nonalcoholic fatty liver disease; Nonalcoholic steatohepatitis; Myofibroblasts; Fibrosis; Antifibrotic pharmacotherapy; Nonalcoholic fatty liver disease treatment strategies; Emerging treatments for nonalcoholic steatohepatitis

Core Tip: Non-alcoholic fatty liver disease (NAFLD) global incidence is escalating significantly. NAFLD covers a range of liver conditions, from simple steatosis to the more severe form known as non-alcoholic steatohepatitis, which involves chronic liver inflammation and the transformation of hepatic stellate cells into myofibroblasts that generate excess extracellular matrix, leading to fibrosis. Hepatocyte ballooning is a key catalyst for fibrosis progression.