Introduction: Mitochondria (mt) are protein-protein interaction (PPI) hubs in the cell where mt-localized and associated proteins interact in a fashion critical for cell fitness. Altered mtPPIs are linked to neurodegenerative disorders (NDs) and drivers of pathological associations to mediate ND progression. Mapping altered mtPPIs will reveal how mt dysfunction is linked to NDs.Areas covered: This review discusses how database sources reflect on the number of mt protein or interaction predictions, and serves as an update on mtPPIs in mt dynamics and homeostasis. Emphasis is given to mRNA expression profiles for mt proteins in human tissues, cellular models relevant to NDs, and altered mtPPIs in NDs such as Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS) and Alzheimer's disease (AD).Expert opinion: We highlight the scarcity of biomarkers to improve diagnostic accuracy and tracking of ND progression, obstacles in recapitulating NDs using human cellular models to underpin the pathophysiological mechanisms of disease, and the shortage of mt protein interactome reference database(s) of neuronal cells. These bottlenecks are addressed by improvements in induced pluripotent stem cell creation and culturing, patient-derived 3D brain organoids to recapitulate structural arrangements of the brain, and cell sorting to elucidate mt proteome disparities between cell types.

中文翻译：

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点错了：线粒体蛋白质间相互作用和神经退行性疾病中的作用改变。

简介：线粒体（mt）是细胞中蛋白质-蛋白质相互作用（PPI）的枢纽，其中mt定位的和相关的蛋白质以对细胞适应性至关重要的方式相互作用。改变的mtPPI与神经退行性疾病（ND）和病理协会的驱动因素有关，以介导ND的进展。映射改变的mtPPIs将揭示mt功能障碍与ND的联系。涵盖的领域：本综述讨论数据库来源如何反映mt蛋白的数量或相互作用预测，并作为mtPPI在mt动态和体内平衡方面的更新。重点关注人体组织中mt蛋白的mRNA表达谱，与ND相关的细胞模型以及ND中改变的mtPPI，例如帕金森氏病（PD），肌萎缩性侧索硬化症（ALS）和阿尔茨海默氏病（AD）。我们强调了缺乏生物标志物以提高诊断准确性和追踪ND进程，使用人类细胞模型来支持疾病的病理生理机制概述ND的障碍以及神经元细胞的mt蛋白相互作用组参考数据库的短缺。通过改进诱导多能干细胞的创建和培养，患者衍生的3D脑类器官来概括大脑的结构安排以及细胞分选来阐明细胞类型之间的mt蛋白质组差异，可以解决这些瓶颈。