Liu JR, Zhao L, Niu QH, Cai JZ, Liu HY. Mechanisms and treatment of metabolic dysfunction-associated fatty liver disease after liver transplantation. World J Gastrointest Surg 2026; 18(8): 121285 [DOI: 10.4240/wjgs.121285]
Corresponding Author of This Article
Liu Zhao, MD, Doctor, Department of Liver Center, The Affiliated Hospital of Qingdao University, No. 59 Haier Road, Laoshan District, Qingdao 266000, Shandong Province, China. zhaoliuqdfy@163.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
review-article
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/
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Share the Article
Liu JR, Zhao L, Niu QH, Cai JZ, Liu HY. Mechanisms and treatment of metabolic dysfunction-associated fatty liver disease after liver transplantation. World J Gastrointest Surg 2026; 18(8): 121285 [DOI: 10.4240/wjgs.121285]
World J Gastrointest Surg. Aug 27, 2026; 18(8): 121285 Published online Aug 27, 2026. doi: 10.4240/wjgs.121285
Mechanisms and treatment of metabolic dysfunction-associated fatty liver disease after liver transplantation
Jun-Rong Liu, Liu Zhao, Qing-Hui Niu, Jin-Zhen Cai, Han-Yun Liu
Jun-Rong Liu, Qingdao Medical College, Qingdao University, Qingdao 266071, Shandong Province, China
Liu Zhao, Qing-Hui Niu, Department of Liver Center, The Affiliated Hospital of Qingdao University, Qingdao 266000, Shandong Province, China
Jin-Zhen Cai, Division of Hepatology, Liver Disease Center, The Affiliated Hospital of Qingdao University, Qingdao 266000, Shandong Province, China
Han-Yun Liu, Department of Infectious Diseases, The Affiliated Hospital of Qingdao University, Qingdao 266000, Shandong Province, China
Co-corresponding authors: Liu Zhao and Qing-Hui Niu.
Author contributions: Liu JR searched for references, created the review, supervised the research, and made critical revisions to the manuscript; Zhao L, Niu QH, Cai JZ and Liu HY conducted the literature review, performed the analysis, interpreted data and drafted the original manuscript; Zhao L is the first corresponding author, and Niu QH is the second corresponding author; all authors helped to prepare the draft manuscript and approved the submitted version.
AI contribution statement: ChatGPT was used only for language polishing during manuscript preparation. The authors fully reviewed and revised the output and take full responsibility for the content of the manuscript. No AI tools were used for study design, data analysis, interpretation, or generation of scientific conclusions. The manuscript was subsequently edited by a professional language editing service.
Supported by National Natural Science Foundation of China, No. 82300665.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Liu Zhao, MD, Doctor, Department of Liver Center, The Affiliated Hospital of Qingdao University, No. 59 Haier Road, Laoshan District, Qingdao 266000, Shandong Province, China. zhaoliuqdfy@163.com
Received: March 23, 2026 Revised: April 23, 2026 Accepted: May 19, 2026 Published online: August 27, 2026 Processing time: 149 Days and 17.9 Hours
Abstract
Metabolism dysfunction-associated fatty liver disease (MAFLD) has emerged as a frequent complication for liver transplant (LT) recipients. In view of the high incidence of MAFLD after LT, research on MAFLD is of considerable clinical significance. Key research areas include the mechanisms responsible for the development of MAFLD following LT, therapeutic strategies, and the optimization of immunosuppressive regimens to achieve a balance between graft protection and metabolic protection. Most existing studies relating to MAFLD following LT are clinical observational studies, and the majority of investigations into pharmacological aspects are based on non-transplantation populations, thus highlighting significant gaps in research. In this review, we propose that the development of MAFLD after LT is primarily driven by the use of immunosuppressive agents and comprehensively synthesize the existing evidence regarding pathogenesis, immunosuppressive optimization strategies, and therapeutic approaches. Specifically, we focus on mechanistic analyses centered on insulin resistance pathways to elucidate immunosuppression-related mechanisms underlying the development and progression of MAFLD following LT. Based on the evaluation of current immunosuppressive optimization strategies and therapeutic agents, we propose several important directions for future research: Optimizing immunosuppressive regimens, conducting transplant recipient-specific pharmacological studies, and exploring strategies to balance metabolic protection with graft preservation.
Core Tip: Metabolism dysfunction-associated fatty liver disease has become a prevalent complication following liver transplantation, appearing as either de novo or recurrent disease. The long-term use of immunosuppressants, specifically glucocorticoids, calcineurin inhibitors, and mammalian target of rapamycin inhibitors, serves as a primary driver of metabolic syndrome by disrupting glucose and lipid homeostasis. In this review, we delineate the synergistic mechanisms of drug-induced insulin resistance, hypertension, and dyslipidemia that promote hepatic steatosis. Management requires a multi-faceted strategy integrating lifestyle modifications, targeted metabolic pharmacotherapy and the optimization of immunosuppressive regimens to balance graft protection with metabolic health.
