Mitochondrial dysregulation is a pivotal hallmark of aging-related disorders. Although there is a considerable understanding of the molecular counteracting responses toward damaged mitochondria, the molecular underpinnings connecting the abnormal aggregation of mitochondrial precursor protein fragments and abrogation of mitochondrial import machinery are far from clear. Recently, proteasomal-dependent degradation was unveiled as a pivotal fine-tuner of TOM machinery-dependent mitochondrial import. Herein, the role of proteasomal-mediated degradation in regulating fidelity of TOM-dependent import is briefly discussed and analyzed. The insights obtained from the characterization of this process may be applied to targeting mitochondrial import dysfunction in some neurodegenerative disorders.

中文翻译：

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蛋白质降解如何调节TOM机械依赖的线粒体输入？

线粒体失调是衰老相关疾病的关键标志。尽管对破坏线粒体的分子抵消反应有了相当大的了解，但连接线粒体前体蛋白片段的异常聚集和线粒体导入机制的废除的分子基础尚不清楚。最近，蛋白酶体依赖性降解被揭示为TOM机械依赖性线粒体输入的关键微调器。在此，简要讨论并分析了蛋白酶体介导的降解在调节TOM依赖性进口保真度中的作用。从此过程的表征中获得的见识可应用于靶向某些神经退行性疾病中的线粒体输入功能障碍。