细胞凋亡
神经生长因子IB
疾病
线粒体
粒线体疾病
癌症研究
细胞生物学
医学
生物
线粒体DNA
遗传学
内科学
转录因子
基因
核受体
作者
Ruihai Fu,Dandan Ling,Qiqi Zhang,Aifang Jiang,Haiyan Pang
标识
DOI:10.1016/j.biopha.2025.118091
摘要
The role of mitochondria in disease development cannot be overlooked, and the targeting of mitochondria for the treatment of disease has emerged as a significant area of research in recent years. Mitochondria are the control center of the intrinsic apoptotic pathway, and their normal functions are finely regulated by a series of complex mechanisms. The nuclear receptor Nur77 is closely related to the functions of the mitochondria and is an active pro-apoptotic member of the nuclear receptor superfamily. The translocation of Nur77 to the mitochondria can promote the conversion of the anti-apoptotic protein Bcl-2 to a pro-apoptotic state, disrupt the balance between mitochondrial fission and fusion, and inhibit mitophagy. These effects lead to irreversible damage to mitochondria and apoptosis, ultimately accelerating the progression of the disease. Here, we review the mechanism and targeted drug development of the mitochondrial apoptosis pathway activated by Nur77 in human diseases, helping to understand the new advances in disease treatment.
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