| Osteoporosis is a systemic bone disease characterized by low bone mass, deterioration in bone microarchitecture, increased bone fragility and fracture prone. It is more common in postmenopausal women and elderly men. Osteoporosis is a degenerative disease and the risk of suffering the disease increases with age. China have the largest number of elderly people in the world. With the prolonged life expectancy and the advent of an aging society, osteoporosis has become an important health problem in our society. N6-methyladenosine (m6A) is a dynamic methylation modification at the N6 site of adenosine. m6A is the most common internal modification in eukaryotic mRNA, which mediates many metabolic processes of mRNA such as splicing, structure conversion, transport, translation, and degradation. It is catalyzed by the methyltransferase complex and this process can be reversed by the FTO and ALKBH5, two demethylases of m6A. The "reader" proteins of m6A function by recognizing the m6A sites. Bone mesenchymal stem cells (BMSCs) are derived from bone marrow and have multi-directional differentiation potentials such as osteoblasts, chondrocytes and adipocytes. m6A can regulate the switch between adipogenic and osteogenic differentiation of BMSCs. As the core of methyltransferase complex, METTL3 can promote the osteogenic differentiation of BMSCs and inhibit their adipogenic differentiation while FTO does the opposite. Various pathways are involved in the process of m6A regulating osteogenic differentiation of BMSCs such as PI3K-Akt pathway, Notch pathway and so on. m6A also can regulate the occurrence of osteoporosis. Both METTL3 and FTO play a vital role in bone formation and they may mediate type Ⅰ osteoporosis and typeⅡosteoporosis respectively. In this systematic review, we summarize the latest research results on the relationship between m6A and differentiation of BMSCs and osteoporosis and determine that m6A may be a therapeutic target of osteoporosis. |