线粒体相关膜蛋白与自噬的相互作用:对神经退行性变的影响

IF 3.9 3区 生物学 Q2 CELL BIOLOGY Mitochondrion Pub Date : 2024-03-20 DOI:10.1016/j.mito.2024.101874
Prakash G. Kulkarni , Vaibhavi M. Mohire , Pranjal P. Waghmare , Tanushree Banerjee
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引用次数: 0

摘要

自从发现ER和线粒体之间的膜接触点(称为线粒体相关膜(MAMs))以来,一些证据确定了它们在调节不同细胞过程(如钙离子信号、线粒体转运和动态、ER应激、炎症、葡萄糖稳态和自噬)中的作用。研究发现,这些膜的完整性对维持这些细胞功能至关重要。越来越多的证据表明,MAMs 是自噬体形成的平台。然而,MAMs 结构的改变与神经退行性疾病的进展有关。自噬失调是神经退行性疾病的标志。在这篇综述中,我们重点介绍了有关 MAMs、其结构组成及其在不同细胞功能中作用的现有知识。我们还讨论了 MAMs 蛋白与自噬功能受损之间的关联,以及它们在阿尔茨海默病和帕金森病等神经退行性疾病进展过程中的参与作用。
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Interplay of mitochondria-associated membrane proteins and autophagy: Implications in neurodegeneration

Since the discovery of membrane contact sites between ER and mitochondria called mitochondria-associated membranes (MAMs), several pieces of evidence identified their role in the regulation of different cellular processes such as Ca2+ signalling, mitochondrial transport, and dynamics, ER stress, inflammation, glucose homeostasis, and autophagy. The integrity of these membranes was found to be essential for the maintenance of these cellular functions. Accumulating pieces of evidence suggest that MAMs serve as a platform for autophagosome formation. However, the alteration within MAMs structure is associated with the progression of neurodegenerative diseases. Dysregulated autophagy is a hallmark of neurodegeneration. Here, in this review, we highlight the present knowledge on MAMs, their structural composition, and their roles in different cellular functions. We also discuss the association of MAMs proteins with impaired autophagy and their involvement in the progression of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease.

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来源期刊
Mitochondrion
Mitochondrion 生物-细胞生物学
CiteScore
9.40
自引率
4.50%
发文量
86
审稿时长
13.6 weeks
期刊介绍: Mitochondrion is a definitive, high profile, peer-reviewed international research journal. The scope of Mitochondrion is broad, reporting on basic science of mitochondria from all organisms and from basic research to pathology and clinical aspects of mitochondrial diseases. The journal welcomes original contributions from investigators working in diverse sub-disciplines such as evolution, biophysics, biochemistry, molecular and cell biology, genetics, pharmacology, toxicology, forensic science, programmed cell death, aging, cancer and clinical features of mitochondrial diseases.
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