线粒体
生物
线粒体DNA
癌症
DNAJA3公司
癌症研究
疾病
线粒体融合
癌症治疗
生物信息学
DNA损伤
癌细胞
平衡
粒线体疾病
瓦博格效应
癌症治疗
功能(生物学)
细胞生物学
自噬
能量稳态
评论文章
作者
Hongling Zhong,Renjie Pan,Yuzhen Ouyang,Tengfei Xiao,Wangning Gu,Hongmin Yang,Hui Wang,Hucheng Li,Tianfang Peng,Pan Chen
标识
DOI:10.1186/s12943-026-02571-3
摘要
Mitochondria are central to health and disease by precisely regulating metabolism and interacting closely with other organelles. Mitochondrial dysfunction contributes to the initiation and development of numerous diseases, including cancer. In cancer cells, metabolic reprogramming, impaired mitochondrial quality control, and mitochondrial DNA damage are linked to tumor initiation, development, and metastasis. Dysregulated mitochondrial function in cells within the tumor microenvironment, such as CD8 + T cells, also promotes cancer progression. Therapeutic approaches targeting mitochondria range from dietary interventions to small-molecule drugs aimed at restoring mitochondrial dysfunction. In this review, we summarize the relationships between mitochondrial dysfunction and cancer from the perspectives of metabolism, quality control, mitochondrial DNA stability, ion homeostasis, and the tumor microenvironment. We also provide updates on mitochondria-targeted therapies, highlighting key translational gaps from bench to bedside. Finally, we discuss future directions for mitochondria-targeted cancer therapy, emphasizing mitochondrial homeostasis as a critical target for improving therapeutic outcomes.
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