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N6-甲基腺苷与自噬在骨骼和组织退变调节中的相互作用。

Interaction between N6-methyladenosine and autophagy in the regulation of bone and tissue degeneration.

作者信息

Wen Xiaodong, Wang Junhu, Wang Qiong, Liu Peilong, Zhao Hongmou

机构信息

Department of Foot and Ankle Surgery, Honghui Hospital of Xi'an Jiaotong University, Xi'an, China.

出版信息

Front Bioeng Biotechnol. 2022 Aug 22;10:978283. doi: 10.3389/fbioe.2022.978283. eCollection 2022.

Abstract

Bone and tissue degeneration are the most common skeletal disorders that seriously affect people's quality of life. N6-methyladenosine (m6A) is one of the most common RNA modifications in eukaryotic cells, affecting the alternative splicing, translation, stability and degradation of mRNA. Interestingly, increasing number of evidences have indicated that m6A modification could modulate the expression of autophagy-related (ATG) genes and promote autophagy in the cells. Autophagy is an important process regulating intracellular turnover and is evolutionarily conserved in eukaryotes. Abnormal autophagy results in a variety of diseases, including cardiomyopathy, degenerative disorders, and inflammation. Thus, the interaction between m6A modification and autophagy plays a prominent role in the onset and progression of bone and tissue degeneration. In this review, we summarize the current knowledge related to the effect of m6A modification on autophagy, and introduce the role of the crosstalk between m6A modification and autophagy in bone and tissue degeneration. An in-depth knowledge of the above crosstalk may help to improve our understanding of their effects on bone and tissue degeneration and provide novel insights for the future therapeutics.

摘要

骨骼和组织退化是严重影响人们生活质量的最常见骨骼疾病。N6-甲基腺苷(m6A)是真核细胞中最常见的RNA修饰之一,影响mRNA的可变剪接、翻译、稳定性和降解。有趣的是,越来越多的证据表明,m6A修饰可以调节自噬相关(ATG)基因的表达并促进细胞中的自噬。自噬是调节细胞内物质周转的重要过程,在真核生物中具有进化保守性。自噬异常会导致多种疾病,包括心肌病、退行性疾病和炎症。因此,m6A修饰与自噬之间的相互作用在骨骼和组织退化的发生和发展中起着重要作用。在这篇综述中,我们总结了目前关于m6A修饰对自噬影响的相关知识,并介绍了m6A修饰与自噬之间的相互作用在骨骼和组织退化中的作用。深入了解上述相互作用可能有助于提高我们对它们对骨骼和组织退化影响的理解,并为未来的治疗提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/585d/9443517/953b084e21e4/fbioe-10-978283-g001.jpg

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