线粒体氧化磷酸化功能障碍在驱动肿瘤发生发展中作用的研究进展  

The research progress on the role of mitochondrial oxidative phosphorylation dysfunction in driving tumorigenesis and development

作　　者：谢文丽 凤志慧[1] XIE Wenli;FENG Zhihui(Department of Occupational Health and Occupational Medicine,School of Public Health,Shandong University,Shandong Jinan 250012,China)

机构地区：[1]山东大学公共卫生学院职业卫生与职业医学系,山东济南250012

出　　处：《现代肿瘤医学》2025年第5期850-856,共7页Journal of Modern Oncology

基　　金：国家自然科学基金(编号:82173460,82373518)。

摘　　要：目前已有研究报道线粒体呼吸在控制表观遗传方面发挥关键作用,进一步研究揭示线粒体呼吸功能障碍能改变高度分化的正常细胞的新陈代谢途径,重塑表观遗传,导致正常细胞发生去分化,使其向肿瘤细胞转化,驱动肿瘤的发生。随着对线粒体-表观遗传调控轴在肿瘤发生发展研究的深入,线粒体和表观基因组有望成为肿瘤治疗的新靶点。该文主要综述线粒体氧化磷酸化功能异常诱发的表观遗传重塑在驱动肿瘤发生发展中作用的研究进展,旨在为肿瘤防治提供更有临床价值的新思路和新方法。It has been reported that mitochondrial respiration plays a key role in controlling epigenetic inheritance,and further studies reveal that mitochondrial respiratory dysfunction can alter the metabolic pathways of highly differentiated somatic cells,remodeling epigenetic inheritance and leading to the dedifferentiation of somatic cells,which transforms them into tumor cells and drives tumorigenesis.With the in-depth study of the mitochondrial-epigenetic regulatory axis in tumorigenesis and development,mitochondria and epigenome are expected to become new targets for tumor therapy.This article mainly reviews the research progress on the role of mitochondrial oxidative phosphorylation function abnormality-induced epigenetic remodeling in driving tumorigenesis and development,aiming to provide new ideas and methods of more clinical value for tumor prevention and treatment.

关 键 词：肿瘤 线粒体 代谢重编程 表观遗传 

分 类 号：R730[医药卫生—肿瘤]