关键词: aging epigenetics m(6)A methylation regeneration sarcopenia skeletal muscle

来  源:   DOI:10.1016/j.biopha.2024.117041

Abstract:
The modification of RNA through the N6-methyladenosine (m6A) has emerged as a growing area of research due to its regulatory role in gene expression and various biological processes regulating the expression of genes. m6A RNA methylation is a post-transcriptional modification that is dynamic and reversible and found in mRNA, tRNA, rRNA, and other non-coding RNA of most eukaryotic cells. It is executed by special proteins known as \"writers,\" which initiate methylation; \"erasers,\" which remove methylation; and \"readers,\" which recognize it and regulate the expression of the gene. Modification by m6A regulates gene expression by affecting the splicing, translation, stability, and localization of mRNA. Aging causes molecular and cellular damage, which forms the basis of most age-related diseases. The decline in skeletal muscle mass and functionality because of aging leads to metabolic disorders and morbidities. The inability of aged muscles to regenerate and repair after injury poses a great challenge to the geriatric populace. This review seeks to explore the m6A epigenetic regulation in the myogenesis and regeneration processes in skeletal muscle as well as the progress made on the m6A epigenetic regulation of aging skeletal muscles.
摘要:
通过N6-甲基腺苷(m6A)修饰RNA已成为一个不断发展的研究领域,因为它在基因表达和调节基因表达的各种生物过程中的调节作用。m6ARNA甲基化是一种动态和可逆的转录后修饰,在mRNA中发现,tRNA,rRNA,和大多数真核细胞的其他非编码RNA。它是由被称为“作家”的特殊蛋白质执行的,“启动甲基化;”橡皮擦,“去除甲基化;和”读者,“识别它并调节基因的表达。m6A修饰通过影响剪接来调节基因表达,翻译,稳定性,和mRNA的定位。衰老导致分子和细胞损伤,这构成了大多数与年龄有关的疾病的基础。由于衰老而导致的骨骼肌质量和功能的下降导致代谢紊乱和发病率。老年肌肉在受伤后无法再生和修复,这对老年人构成了巨大挑战。本文旨在探讨m6A在骨骼肌肌发生和再生过程中的表观遗传调控,以及m6A在衰老骨骼肌中的表观遗传调控研究进展。
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