Yue Xi, Dong Guo, Shi Li, Jie-Yu Guo, Jing-Feng Tang, Ce-Fan Zhou, School of Life and Health Sciences, Institute of Biomedical Research, National “111” Center for Cellular Regulation and Molecular Pharmaceutics, Key Laboratory of Fermentation Engineering (Ministry of Education), Hubei University of Technology, Wuhan 430068, Hubei Province, China
Xing-Zhen Chen, Department of Physiology, University of Alberta, Edmonton, AB T6G 2R3, Canada
Co-first authors: Yue Xi and Dong Guo.
Co-corresponding authors: Jing-Feng Tang and Ce-Fan Zhou.
Author contributions: Xi Y and Guo D contributed equally to this study as co-first authors; Tang JF and Zhou CF contributed equally to this study as co-corresponding authors; Xi Y prepared the original draft; Zhou CF and Guo D contributed to the conceptualization, writing, review and editing of the manuscript; Xi Y, Li S, Zhou CF and Tang JF collaboratively drafted the manuscript; Guo JY and Chen XZ provided some valuable opinions; all authors have reviewed and approved the final version of the manuscript.
Conflict-of-interest statement: Dr. Zhou has nothing to disclose.
Corresponding author: Ce-Fan Zhou, School of Life and Health Sciences, Institute of Biomedical Research, National “111” Center for Cellular Regulation and Molecular Pharmaceutics, Key Laboratory of Fermentation Engineering (Ministry of Education), Hubei University of Technology, No. 28 Nanli Road, Wuhan 430068, Hubei Province, China. cefan@hbut.edu.cn
Received: December 24, 2024 Revised: February 25, 2025 Accepted: March 6, 2025 Published online: April 7, 2025 Processing time: 99 Days and 22.8 Hours
Core Tip
Core Tip: The mixed lineage kinase domain-like protein (MLKL) ATP-binding pocket inhibitor CPD4 demonstrates significant promise as a novel therapeutic agent for alcoholic liver disease (ALD), providing dual benefits through the reduction of hepatic inflammation and the enhancement of liver function. In this article, we emphasize the regulatory role of CPD4 as a targeted inhibitor of the MLKL ATP-binding pocket and highlight its ability to modulate ALD progression through the NF-κB signaling pathway. Furthermore, future research should explore the potential of combination therapies involving MLKL inhibitors to optimize treatment strategies. These advancements may pave the way for personalized approaches to treating ALD and other related liver diseases.
