m6A Methylation Regulates Osteoblastic Differentiation and Bone Remodeling

Mei Huang, Shaozhe Xu, Lifei Liu, Miao Zhang, Jianmin Guo, Yu Yuan, Jiake Xu, Xi Chen, Jun Zou

Research output: Contribution to journalReview articlepeer-review

16 Citations (Scopus)

Abstract

Osteoporosis is a prevalent bone disease of the aging population, which is characterized by a decrease in bone mass because of the imbalance of bone metabolism. Although the prevention and treatment of osteoporosis have been explored by different researchers, the mechanisms underlying osteoporosis are not clear exactly. N6 methyladenosine (m6A) is a methylated adenosine nucleotide, which functions through its interaction with the proteins called “writers,” “readers” and “erasers.” The epigenetic regulation of m6A has been demonstrated to affect mRNA processing, nuclear export, translation, and splicing. At the cellular level, m6A modification has been known to affect cell proliferation, differentiation, and apoptosis of bone-related cells, such as bone marrow mesenchymal stem cells (BMSC), osteoblasts, and osteoclasts by regulating the expression of ALP, Runx2, Osterix, VEGF, and other related genes. Furthermore, PTH/Pth1r, PI3K‐Akt, Wnt/β‐Catenin, and other signaling pathways, which play important roles in the regulation of bone homeostasis, are also regulated by m6A. Thus, m6A modification may provide a new approach for osteoporosis treatment. The key roles of m6A modification in the regulation of bone health and osteoporosis are reviewed here in this article.

Original languageEnglish
Article number783322
JournalFrontiers in Cell and Developmental Biology
Volume9
DOIs
Publication statusPublished - 21 Dec 2021

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