Osteoporosis is a systemic bone disease in which bone density and bone quality are reduced due to various reasons, bone microstructure is destroyed, and bone fragility is increased, which is prone to fractures.

The disease mostly occurs in middle-aged and elderly people. After suffering from osteoporosis, middle-aged and elderly people are prone to pain in the waist and legs. In severe cases, the spine deforms and fractures cause disability. Finally, it leads to restricted activities, inability to take care of themselves, and greatly reduces the quality of life. The cost of treatment also brings a heavy financial burden to individuals and families.

In recent years, some researchers had claimed that β-Nicotinamide mononucleotide (short name: NMN, CAS No.: 1094-61-7) can promote the expansion of mesenchymal stem cells (MSC) through the SIRT 1 pathway, stimulate osteogenic differentiation and inhibit adipocyte differentiation, and slow down bone loss. This may propose a new plan for the treatment of osteoporosis.

MSC is the "star member" of the stem cell family. It has self-replication and multi-directional differentiation potential, and can differentiate into mature cells, chondrocytes, and adipocytes. Mesenchymal stromal cells (MSC) can differentiate into various types of cells, including osteoblasts, chondrocytes and adipocytes. The flexibility of this cell contributes to the wide clinical application of MSC in tissue repair. However, effective cell expansion of MSCs for stem cell therapy still faces challenges. Current MSC culture methods have led to reduced MSC self-renewal and compromised treatment results. This study shows that nicotinamide mononucleotide (NMN) is a key natural NAD + intermediate, which effectively promotes the expansion of MSC in vitro and in vivo. MSCs expanded in vitro enhanced osteogenic effects, but reduced fat formation. In addition, supplementation of NMN stimulates the osteogenesis of endogenous MSCs and protects the bones from aging and radiation-induced damage in mice. In terms of mechanism, we found that NMN treatment up-regulated SIRT1. By using Prx1 cre to overexpress SIRT1 in MSC; ColA1 flox-stop-flox-SIRT1 mice promoted the osteogenic effect of adult mice and reduced fat formation. Overall, scientific research data show that NMN promotes the self-renewal of MSCs in aging mice by up-regulating SIRT1, enhances osteogenesis and reduces fat formation.

These studies will play a very important role in the treatment and prevention of osteoporosis in the future.

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