The Potential of Targeting Autophagy-Related Non-coding RNAs in the Treatment of Alzheimer's and Parkinson's Diseases.

IF 3.6 4区 医学 Q3 CELL BIOLOGY
Abdolkarim Talebi Taheri, Zakieh Golshadi, Hamidreza Zare, Azam Alinaghipour, Zahra Faghihi, Ehsan Dadgostar, Zeinab Tamtaji, Michael Aschner, Hamed Mirzaei, Omid Reza Tamtaji, Fatemeh Nabavizadeh
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Abstract

Clearance of accumulated protein aggregates is one of the functions of autophagy. Recently, a clearer understanding of non-coding RNAs (ncRNAs) functions documented that ncRNAs have important roles in several biological processes associated with the development and progression of neurodegenerative disorders. Subtypes of ncRNA, including microRNA (miRNA), long noncoding RNA (lncRNA), and circular RNA (circRNA), are commonly dysregulated in neurodegenerative disorders such as Alzheimer and Parkinson diseases. Dysregulation of these non-coding RNAs has been associated with inhibition or stimulation of autophagy. Decreased miR-124 led to decreased/increased autophagy in experimental model of Alzheimer and Parkinson diseases. Increased BACE1-AS showed enhanced autophagy in Alzheimer disease by targeting miR-214-3p, Beclin-1, LC3-I/LC3-II, p62, and ATG5. A significant increase in NEAT1led to stimulated autophagy in experimental model of PD by targeting PINK1, LC3-I, LC3-II, p62 and miR-374c-5p. In addition, increased BDNF-AS and SNHG1 decreased autophagy in MPTP-induced PD by targeting miR-125b-5p and miR-221/222, respectively. The upregulation of circNF1-419 and circSAMD4A resulted in an increased autophagy by regulating Dynamin-1 and miR-29c 3p, respectively. A detailed discussion of miRNAs, circRNAs, and lncRNAs in relation to their autophagy-related signaling pathways is presented in this study.

Abstract Image

以自噬相关非编码 RNA 为靶点治疗阿尔茨海默氏症和帕金森氏症的潜力》(The Potential of Targeting Autophagy-Related Non-coding RNAs in the Treatment of Alzheimer's and Parkinson's Diseases.
清除累积的蛋白质聚集体是自噬的功能之一。最近,人们对非编码 RNA(ncRNA)功能有了更清晰的认识,发现 ncRNA 在与神经退行性疾病的发生和发展相关的几个生物学过程中发挥着重要作用。包括微小核糖核酸(miRNA)、长非编码核糖核酸(lncRNA)和环状核糖核酸(circRNA)在内的 ncRNA 亚型通常在阿尔茨海默病和帕金森病等神经退行性疾病中出现失调。这些非编码 RNA 的失调与抑制或刺激自噬有关。在阿尔茨海默病和帕金森病的实验模型中,miR-124 的减少导致自噬的减少/增加。通过靶向 miR-214-3p、Beclin-1、LC3-I/LC3-II、p62 和 ATG5,BACE1-AS 的增加增强了阿尔茨海默病的自噬作用。通过靶向 PINK1、LC3-I、LC3-II、p62 和 miR-374c-5p,NEAT1 的显着增加促进了老年痴呆症实验模型的自噬。此外,BDNF-AS和SNHG1的增加分别通过靶向miR-125b-5p和miR-221/222降低了MPTP诱导的帕金森病的自噬。circNF1-419和circSAMD4A的上调分别通过调节Dynamin-1和miR-29c 3p导致自噬增加。本研究详细讨论了 miRNA、circRNA 和 lncRNA 与自噬相关信号通路的关系。
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来源期刊
CiteScore
7.70
自引率
0.00%
发文量
137
审稿时长
4-8 weeks
期刊介绍: Cellular and Molecular Neurobiology publishes original research concerned with the analysis of neuronal and brain function at the cellular and subcellular levels. The journal offers timely, peer-reviewed articles that describe anatomic, genetic, physiologic, pharmacologic, and biochemical approaches to the study of neuronal function and the analysis of elementary mechanisms. Studies are presented on isolated mammalian tissues and intact animals, with investigations aimed at the molecular mechanisms or neuronal responses at the level of single cells. Cellular and Molecular Neurobiology also presents studies of the effects of neurons on other organ systems, such as analysis of the electrical or biochemical response to neurotransmitters or neurohormones on smooth muscle or gland cells.
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