利用Nur77的线粒体凋亡途径:一种有前途的靶向疾病干预治疗策略

IF 6.9 2区 医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL
Ruihai Fu , Dandan Ling , Qiqi Zhang , Aifang Jiang , Haiyan Pang
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引用次数: 0

摘要

线粒体在疾病发展中的作用不容忽视,近年来靶向线粒体治疗疾病已成为一个重要的研究领域。线粒体是细胞凋亡内在通路的调控中心,其正常功能受到一系列复杂机制的精细调控。核受体Nur77与线粒体的功能密切相关,是核受体超家族中一个活跃的促凋亡成员。Nur77易位到线粒体可以促进抗凋亡蛋白Bcl-2向促凋亡状态转化,破坏线粒体裂变与融合的平衡,抑制线粒体自噬。这些影响导致线粒体和细胞凋亡的不可逆损伤,最终加速疾病的进展。本文综述了由Nur77激活的线粒体凋亡通路在人类疾病中的作用机制和靶向药物开发,有助于了解疾病治疗的新进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Harnessing Nur77's mitochondrial apoptotic pathway: A promising therapeutic strategy for targeted disease intervention
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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来源期刊
CiteScore
11.90
自引率
2.70%
发文量
1621
审稿时长
48 days
期刊介绍: Biomedicine & Pharmacotherapy stands as a multidisciplinary journal, presenting a spectrum of original research reports, reviews, and communications in the realms of clinical and basic medicine, as well as pharmacology. The journal spans various fields, including Cancer, Nutriceutics, Neurodegenerative, Cardiac, and Infectious Diseases.
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