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Long Non-coding RNAs, Novel Culprits, or Bodyguards in Neurodegenerative Diseases.
Molecular Therapy - Nucleic Acids ( IF 6.5 ) Pub Date : 2017-12-22 , DOI: 10.1016/j.omtn.2017.12.011
Ding-Qi Wang 1 , Peng Fu 2 , Chengye Yao 3 , Ling-Shuang Zhu 1 , Tong-Yao Hou 1 , Jian-Guo Chen 4 , Youming Lu 5 , Dan Liu 6 , Ling-Qiang Zhu 7
Affiliation  

Long non-coding RNA (lncRNA) is a kind of non-coding RNA (ncRNA), with a length of 200 nt to 100 kb, that lacks a significant open reading frame (ORF) encoding a protein. lncRNAs are widely implicated in various physiological and pathological processes, such as epigenetic regulation, cell cycle regulation, cell differentiation regulation, cancer, and neurodegenerative diseases, through their interactions with chromatin, protein, and other RNAs. Numerous studies have suggested that lncRNAs are closely linked with the occurrence and development of a variety of diseases, especially neurodegenerative diseases, of which the etiologies are complicated and the underlying mechanisms remain elusive. Determining the roles of lncRNA in the pathogenesis of neurodegenerative diseases will not only deepen understanding of the physiological and pathological processes that occur in those diseases but also provide new ideas and solutions for their diagnosis and prevention. This review aims to highlight the progress of lncRNA research in the pathological and behavioral changes of neurodegenerative diseases. Specifically, we focus on how lncRNA dysfunctions are involved in the pathogenesis of Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis.



中文翻译:

神经退行性疾病中的长非编码RNA,新型罪犯或保镖。

长非编码RNA(lncRNA)是一种非编码RNA(ncRNA),长度为200 nt至100 kb,缺少编码蛋白质的显着开放阅读框(ORF)。lncRNA通过与染色质,蛋白质和其他RNA的相互作用而广泛参与各种生理和病理过程,例如表观遗传调控,细胞周期调控,细胞分化调控,癌症和神经退行性疾病。大量研究表明,lncRNA与多种疾病(尤其是神经退行性疾病)的发生和发展密切相关,这些疾病的病因复杂且潜在机制尚不清楚。确定lncRNA在神经退行性疾病的发病机理中的作用不仅将加深对这些疾病中发生的生理和病理过程的了解,而且还将为诊断和预防其提供新的思路和解决方案。这篇综述旨在强调lncRNA在神经退行性疾病的病理和行为变化中的研究进展。具体而言,我们关注lncRNA功能异常如何参与阿尔茨海默氏病,帕金森氏病,亨廷顿氏病和肌萎缩性侧索硬化的发病机理。

更新日期:2017-12-22
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