METTL3介导m6A甲基化对骨代谢及骨质疏松的调控作用
Regulation of METTL3-mediated m6A methylation on bone metabolism and osteoporosis
  
DOI:10.3969/j.issn.1006-7108.2024.11.022
中文关键词:  METTL3  m6A甲基化  骨代谢  骨质疏松
英文关键词:METTL3  m6A methylation  bone metabolism  osteoporosis
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黄媚1,2 马常宁1 张苗1* 1.燕山大学体育学院河北 秦皇岛 066004 2.温州医科大学康复医学院浙江 温州 325035 
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中文摘要:
      随着社会老龄化和人们生活方式的改变,导致骨质疏松患病率升高,因此对公众健康危害极大。骨质疏松的发病机制及临床治疗方法仍不明确,目前有研究发现N6-甲基腺苷(N6 methyladenosine,m6A)在不改变碱基序列的前提下,甲基化成为调控基因转录水平的重要机制。其中,甲基转移酶样3(methyltransferase-like 3,METTL3)作为一种关键的甲基转移酶,专门催化m6A甲基化修饰。经过对现有文献报道分析发现METTL3在干细胞、成骨细胞以及破骨细胞的增殖、分化及凋亡等多个生物学过程中扮演着重要角色,从而有效地调节和维持了骨代谢的平衡状态。因此,该文通过详细介绍METTL3在骨代谢中的研究现状,为进一步探究骨质疏松的治疗提供新思路。
英文摘要:
      The high prevalence of osteoporosis has recently been extremely hazardous to public health. The pathogenesis and clinical treatment of osteoporosis are still incomplete. Currently,it has been found that N6-methyladenosine (m6A) Without changing the base sequence,methylation becomes an important mechanism to regulate the transcription level of genes. Among them,methyltransferase-like 3 (METTL3),a key methyltransferase, specifically catalyzes m6A methylation modification. After an exhaustive review of the existing literature,we found that METTL3 plays an important role in several biological processes, including proliferation, differentiation and apoptosis of stem cells,osteoblasts and osteoclasts,and thus effectively regulates and maintains the homeostatic state of bone metabolism. Therefore,by detailing the current research of METTL3 in bone metabolism,this paper provides new ideas for further exploration of osteoporosis treatment.
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