Inhibitors of mitochondrial fission as a therapeutic strategy for diseases with oxidative stress and mitochondrial dysfunction.
Inhibitors of mitochondrial fission as a therapeutic strategy for diseases with oxidative stress and mitochondrial dysfunction.
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DOI：
10.3233/jad-132060
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Reddy PH
中科院分区：
文献类型：
--
作者：
Reddy PH
线粒体是细胞内必不可少的细胞器，对细胞的生存和死亡至关重要。最近的线粒体研究表明，线粒体动力学--正常线粒体动力学中分裂与融合的平衡--是真核细胞中一种重要的细胞机制，参与维持线粒体的形态、结构、数量、分布和功能。对线粒体和细胞功能的研究表明，在许多衰老和神经退行性疾病以及几种遗传性线粒体疾病中，线粒体动力学受到损害，这种损害涉及线粒体过度分裂，导致线粒体结构变化和功能障碍，以及细胞损伤。人们试图开发分子来减少线粒体分裂，同时在那些涉及线粒体过度分裂的疾病中保持正常的线粒体融合和功能。本文讨论了哺乳动物细胞正常和疾病状态下线粒体分裂的机制，并讨论了旨在开发治疗方法的研究，如Mdivi、dynasore和p110，以防止或抑制线粒体过度分裂。
Mitochondria are essential cytoplasmic organelles, critical for cell survival and death. Recent mitochondrial research revealed that mitochondrial dynamics – the balance of fission and fusion in normal mitochondrial dynamics – is an important cellular mechanism in eukaryotic cell and is involved in the maintenance of mitochondrial morphology, structure, number, distribution, and function. Research into mitochondria and cell function has revealed that mitochondrial dynamics is impaired in a large number of aging and neurodegenerative diseases, and in several inherited mitochondrial diseases, and that this impairment involves excessive mitochondrial fission, resulting in mitochondrial structural changes and dysfunction, and cell damage. Attempts have been made to develop molecules to reduce mitochondrial fission while maintaining normal mitochondrial fusion and function in those diseases that involve excessive mitochondrial fission. This review article discusses mechanisms of mitochondrial fission in normal and diseased states of mammalian cells and discusses research aimed at developing therapies, such as Mdivi, Dynasore and P110, to prevent or to inhibit excessive mitochondrial fission.