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探讨线粒体功能障碍与帕金森病进展的关系。

Insights on the Correlation between Mitochondrial Dysfunction and the Progression of Parkinson's Disease.

机构信息

Department of Biotechnology, Noida Institute of Engineering and Technology, Noida, India.

出版信息

Endocr Metab Immune Disord Drug Targets. 2024;24(9):1007-1014. doi: 10.2174/0118715303249690231006114308.

Abstract

The aetiology of a progressive neuronal Parkinson's disease has been discussed in several studies. However, due to the multiple risk factors involved in its development, such as environmental toxicity, parental inheritance, misfolding of protein, ageing, generation of reactive oxygen species, degradation of dopaminergic neurons, formation of neurotoxins, mitochondria dysfunction, and genetic mutations, its mechanism of involvement is still discernible. Therefore, this study aimed to review the processes or systems that are crucially implicated in the conversion of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) into its lethal form, which directly blockades the performance of mitochondria, leading to the formation of oxidative stress in the dopaminergic neurons of substantia nigra pars compacta (SNpc) and resulting in the progression of an incurable Parkinson's disease. This review also comprises an overview of the mutated genes that are frequently associated with mitochondrial dysfunction and the progression of Parkinson's disease. Altogether, this review would help future researchers to develop an efficient therapeutic approach for the management of Parkinson's disease via identifying potent prognostic and diagnostic biomarkers.

摘要

几种研究讨论了进行性神经元帕金森病的病因。然而,由于其发展涉及多种风险因素,如环境毒性、父母遗传、蛋白质错误折叠、衰老、活性氧的产生、多巴胺能神经元降解、神经毒素形成、线粒体功能障碍和基因突变,其参与的机制仍然难以确定。因此,本研究旨在综述与 MPTP(1-甲基-4-苯基-1,2,3,6-四氢吡啶)转化为其致死形式密切相关的过程或系统,该过程直接阻断线粒体的功能,导致黑质致密部(SNpc)多巴胺能神经元中氧化应激的形成,并导致不可治愈的帕金森病的进展。这篇综述还包括经常与线粒体功能障碍和帕金森病进展相关的突变基因的概述。总的来说,这篇综述将帮助未来的研究人员通过识别有效的预后和诊断生物标志物,为管理帕金森病开发有效的治疗方法。

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