线粒体功能障碍促进肿瘤恶病质发生的机制研究进展  

Research Progress in Mechanisms of Mitochondrial Dysfunction Promoting Tumor Cachexia

作　　者：唐欣蕊 于新凤[1] 孙于棋 宋雨佳 TANG Xinrui;YU Xinfeng;SUN Yuqi;SONG Yujia(School of Basic Medical Sciences,Capital Medical University,Beijing 100069,China)

机构地区：[1]首都医科大学基础医学院,北京100069

出　　处：《医学综述》2024年第2期193-197,共5页Medical Recapitulate

基　　金：首都医科大学长学制学生基础阶段科研训练项目(7NZDS2021046)。

摘　　要：肿瘤恶病质可累及多器官,严重影响患者生活质量和疾病预后。线粒体功能障碍可通过多种机制促进肿瘤恶病质发生,包括线粒体有氧氧化相关基因异常及Warburg效应导致的能量代谢异常、线粒体生物发生障碍导致的线粒体数量调控异常、线粒体分裂融合障碍导致的线粒体形态改变以及线粒体自噬功能失调导致的炎症反应异常等。因此,全面了解线粒体功能障碍促进肿瘤恶病质发生的机制,可以增强人们对肿瘤恶病质的认知,为改善肿瘤恶病质患者的治疗策略提供科学依据。Tumor cachexia can act on multiple systemic organs,seriously affecting the quality of life and prognosis of the patients.Mitochondrial dysfunction can promote tumor cachexia through a variety of mechanisms,including abnormalities in mitochondrial aerobic oxidation related genes and energy metabolism abnormalities caused by Warburg effect,abnormalities in mitochondrial quantity caused by mitochondrial biogenesis disorders,mitochondrial morphological changes caused by mitochondrial fission and fusion disorders and mitochondrial autophagy dysfunction and subsequent abnormal inflammatory response.Therefore,a comprehensive understanding of the mechanism of mitochondrial dysfunction promoting tumor cachexia can enhance the awareness of tumor cachexia and provide scientific basis for improving treatment strategies for patients with tumor cachexia.

关 键 词：肿瘤 恶病质 线粒体功能障碍 

分 类 号：R730[医药卫生—肿瘤]