改善铜过载所致线粒体功能障碍防治代谢相关脂肪性肝病的研究进展
DOI: 10.12449/JCH251223
利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:方禹彤负责文章的构思与设计,论文撰写;陈依凡、郭碧玉、杨惠栾、白雨桐负责论文修订与审校;姚政、杨晓密指导撰写文章并最后定稿。
Research advances in the prevention and treatment of metabolic associated fatty liver disease by alleviating copper overload-induced mitochondrial dysfunction
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摘要: 铜是人体所必需的微量元素之一,以辅酶或含铜蛋白形式参与线粒体呼吸、能量代谢和抗氧化等过程。细胞内铜蓄积主要表现为铜在线粒体内的异常积聚,导致线粒体形态和功能出现异常。代谢相关脂肪性肝病(MAFLD)的病理进程与线粒体功能障碍密切相关。研究已证实铜过载可以促进MAFLD的发生发展,但关于铜过载导致线粒体功能障碍引发MAFLD的相关机制和药物研究进展,目前尚缺乏系统性总结。基于此,本文系统综述了铜过载引发线粒体功能障碍导致MAFLD的相关机制及药物研究进展,以期为MAFLD进一步的研究和治疗提供理论参考。Abstract: Copper is one of the essential trace elements in the human body and participates in mitochondrial respiration, energy metabolism, and antioxidant processes in the form of coenzymes or copper-containing proteins. Intracellular copper accumulation mainly manifests as abnormal copper accumulation within mitochondria, leading to abnormalities in mitochondrial morphology and function. the pathological process of metabolic associated fatty liver disease (MAFLD) is closely associated with mitochondrial dysfunction. Studies have confirmed that copper overload can promote the development and progression of MAFLD; however, there is still a lack of systematic summarization of the mechanisms by which copper overload induces mitochondrial dysfunction and leads to MAFLD and related advances in drug research. In this context, this article reviews the research advances in the mechanisms by which copper overload induces mitochondrial dysfunction and leads to MAFLD, as well as related advances in drug research, in order to provide a theoretical reference for further investigation and treatment of MAFLD.
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Key words:
- Metabolic Associated Fatty Liver Disease /
- Mitochondria /
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Copper
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