自噬和丝裂噬在神经退行性疾病中的作用

IF 2.7 4区 医学 Q3 NEUROSCIENCES
Lakshay Kapil, Vishal Kumar, Simranjit Kaur, Deepali Sharma, Charan Singh, Arti Singh
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引用次数: 0

摘要

自噬是一种自我毁灭的细胞过程,它能清除细胞内的重要代谢物和废物,从而保持细胞健康。线粒体吞噬(Mitophagy)是自体吞噬造成线粒体内部破坏,并彻底清除受损或受压线粒体的过程,从而增强细胞健康。线粒体是细胞的动力室,发挥着产生 ATP(三磷酸腺苷)、新陈代谢、Ca2+ 缓冲和信号转导等重要功能。许多不同的机制(包括内吞体和自噬体运输)将这些底物带到溶酶体进行处理。自噬过程和内吞过程各有不同的分区,它们动态地相互影响,以完成消化。由于丝裂吞噬对维持细胞健康和利用遗传学、细胞生物学和蛋白质组学技术至关重要,因此有必要了解其起始过程,特别是在泛素和受体依赖性信号在损伤线粒体中的作用。尽管阿尔茨海默病(AD)、帕金森病(PD)、亨廷顿病(HD)和肌萎缩性脊髓侧索硬化症(ALS)的症状和遗传基础相似,但它们都与神经元功能障碍相关的自噬和溶酶体内途径异常有关。线粒体自噬负责线粒体的正常更替,在某些生理或病理情况下,它可能会推动有问题线粒体的清除。由于神经元对能量的需求很高,且起源于有丝分裂后,因此特别容易受到自噬和线粒体功能失常的影响。这篇文章的重点是自噬和线粒体吞噬在神经退行性疾病中的重要性,以及如何利用它们创造治疗各种神经系统疾病的新疗法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of Autophagy and Mitophagy in Neurodegenerative Disorders.

Autophagy is a self-destructive cellular process that removes essential metabolites and waste from inside the cell to maintain cellular health. Mitophagy is the process by which autophagy causes disruption inside mitochondria and the total removal of damaged or stressed mitochondria, hence enhancing cellular health. The mitochondria are the powerhouses of the cell, performing essential functions such as ATP (adenosine triphosphate) generation, metabolism, Ca2+ buffering, and signal transduction. Many different mechanisms, including endosomal and autophagosomal transport, bring these substrates to lysosomes for processing. Autophagy and endocytic processes each have distinct compartments, and they interact dynamically with one another to complete digestion. Since mitophagy is essential for maintaining cellular health and using genetics, cell biology, and proteomics techniques, it is necessary to understand its beginning, particularly in ubiquitin and receptor-dependent signalling in injured mitochondria. Despite their similar symptoms and emerging genetic foundations, Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS) have all been linked to abnormalities in autophagy and endolysosomal pathways associated with neuronal dysfunction. Mitophagy is responsible for normal mitochondrial turnover and, under certain physiological or pathological situations, may drive the elimination of faulty mitochondria. Due to their high energy requirements and post-mitotic origin, neurons are especially susceptible to autophagic and mitochondrial malfunction. This article focused on the importance of autophagy and mitophagy in neurodegenerative illnesses and how they might be used to create novel therapeutic approaches for treating a wide range of neurological disorders.

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来源期刊
CiteScore
5.10
自引率
3.30%
发文量
158
审稿时长
6-12 weeks
期刊介绍: Aims & Scope CNS & Neurological Disorders - Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular targets involved in neurological and central nervous system (CNS) disorders e.g. disease specific proteins, receptors, enzymes, genes. CNS & Neurological Disorders - Drug Targets publishes guest edited thematic issues written by leaders in the field covering a range of current topics of CNS & neurological drug targets. The journal also accepts for publication original research articles, letters, reviews and drug clinical trial studies. As the discovery, identification, characterization and validation of novel human drug targets for neurological and CNS drug discovery continues to grow; this journal is essential reading for all pharmaceutical scientists involved in drug discovery and development.
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