Darya Rajabi, Shaghayegh Khanmohammadi, Nima Rezaei
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引用次数: 0
摘要
肌萎缩性脊髓侧索硬化症(ALS)是一种进行性神经退行性疾病,预后不良,可导致死亡。由于其病理机制复杂,ALS 的诊断和治疗本身就具有挑战性。长非编码 RNA(lncRNA)是指长度超过 200 个核苷酸的转录本,参与不同的细胞过程,尤其是基因表达。近年来,关于lncRNA类别及其在不同疾病病理中的干扰作用的研究越来越多,显示了它们在诊断和治疗神经退行性疾病方面的巨大贡献。在这篇综述中,我们讨论了NEAT1和C9orf72-as等lncRNA在TAR DNA结合蛋白-43(TDP-43)、肉瘤融合蛋白(FUS)、1型超氧化物歧化酶(SOD1)等不同基因突变导致的ALS发病机制中的作用。NEAT1 在 ALS 发病机制中是一个公认的 lncRNA,因此,我们详细阐述了它参与形成副斑块、应激反应、炎症反应和细胞凋亡的情况。此外,我们还讨论了反义 lncRNA(as-lncRNA),这是一组来自基因反向链的关键转录本,包括 ZEB1-AS1 和 ATXN2-AS,它们是 ALS 病理学中新发现的成分。最后,我们回顾了将 lncRNAs 用作生物标记物和治疗药物的现状,以及进一步研究 lncRNA 应用的未来愿景。
The role of long noncoding RNAs in amyotrophic lateral sclerosis.
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease with a poor prognosis leading to death. The diagnosis and treatment of ALS are inherently challenging due to its complex pathomechanism. Long noncoding RNAs (lncRNAs) are transcripts longer than 200 nucleotides involved in different cellular processes, incisively gene expression. In recent years, more studies have been conducted on lncRNA classes and interference in different disease pathologies, showing their promising contribution to diagnosing and treating neurodegenerative diseases. In this review, we discussed the role of lncRNAs like NEAT1 and C9orf72-as in ALS pathogenesis mechanisms caused by mutations in different genes, including TAR DNA-binding protein-43 (TDP-43), fused in sarcoma (FUS), superoxide dismutase type 1 (SOD1). NEAT1 is a well-established lncRNA in ALS pathogenesis; hence, we elaborate on its involvement in forming paraspeckles, stress response, inflammatory response, and apoptosis. Furthermore, antisense lncRNAs (as-lncRNAs), a key group of transcripts from the opposite strand of genes, including ZEB1-AS1 and ATXN2-AS, are discussed as newly identified components in the pathology of ALS. Ultimately, we review the current standing of using lncRNAs as biomarkers and therapeutic agents and the future vision of further studies on lncRNA applications.
期刊介绍:
Reviews in the Neurosciences provides a forum for reviews, critical evaluations and theoretical treatment of selective topics in the neurosciences. The journal is meant to provide an authoritative reference work for those interested in the structure and functions of the nervous system at all levels of analysis, including the genetic, molecular, cellular, behavioral, cognitive and clinical neurosciences. Contributions should contain a critical appraisal of specific areas and not simply a compilation of published articles.