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REVIEW article
Front. Pharmacol.
Sec. Gastrointestinal and Hepatic Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1572592
This article is part of the Research Topic Reviews in Gastrointestinal and Hepatic Pharmacology: 2024 View all 7 articles
Mechanism and therapeutic potential of liver injury induced by cholesterol-associated proteins
Provisionally accepted
Yourong Zhou 1 Yashi Cao 1 Yiming Yin 1
Zhifei Xu 1
Xiaochun Yang 1
Bo Yang 2,3
Peihua Luo 1,4
Hao Yan 1,5*
Qiaojun He 1,3,4- 1 Center for Drug Safety Evaluation and Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang Province, China
- 2 Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang Province, China
- 3 School of Medicine, Hangzhou City University, Hangzhou, China
- 4 Innovation Institute for Artificial Intelligence in Medicine of Zhejiang University, Hangzhou, China
- 5 Zhejiang University, Hangzhou, China
Cholesterol, the most abundant sterol molecule in mammalian organisms, serves not only as a fundamental structural component of cell membranes but also as a critical regulator of cellular signaling and function. Cholesterol-associated proteins can mediate liver injury either directly by influencing cholesterol levels or through non-cholesterol pathways. These non-cholesterol pathways, which operate independently of cholesterol's traditional metabolic functions, are regulated by specific transcription factors ， proteins and receptors. Dysregulation of cholesterol-associated can disrupt cellular homeostasis, leading to liver injury, metabolic disorders, and even tumorigenesis. In this article, we explore the mechanisms by which cholesterol-associated proteins contribute to liver injury via both classical cholesterol pathways and non-cholesterol pathways, and discuss their potential as therapeutic targets for liver-related diseases.
Keywords: cholesterol metabolism, liver injury, cholesterol-related proteins, regulatory factors, therapeutic targets
Received: 07 Feb 2025; Accepted: 07 Mar 2025.
Copyright: © 2025 Zhou, Cao, Yin, Xu, Yang, Yang, Luo, Yan and He. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Hao Yan, Zhejiang University, Hangzhou, China
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