The role of NMN in fracture repair

Recently, the research group of Yifeng Zhang, School of Life Science and Technology, Shanghai University of Science and Technology, and the research group of Zhao Yun, Center of Excellence in Molecular and Cell Science, Chinese Academy of Sciences, cooperated. The paper was published in the academic journal Theranostics with the title "Nicotinamide Mononucleotide enhances fracture healing by promoting skeletal stem cell. The study found that niacinamide mononuclear phosphate (NMN) can promote fracture healing early in injury by promoting stem cell proliferation at the site of fracture callus.

 
Figure 1. The proliferation of bone stem cells in the initial stage of fracture healing is regulated by NAD and influences the formation and eventual healing of cartilage callus

Bone regeneration at broken end after fracture is a complex process dominated by endochondral osteogenesis. The size of cartilage callus is an important index to evaluate the early healing of fracture and the final repair process of broken end.

The formation of chondrocallus originates from the proliferation and differentiation of heterogeneous bone stem cells into chondrocytes at the initial stage of bone injury. However, adverse factors such as aging, smoking and diabetes hinder the expansion of bone injury stem cells, thus hindering the formation of chondrocallus, and ultimately increasing the incidence of delayed or non-union.

The activity of bone stem cells is essential for the healing of bone injury.

NMN is an important biosynthetic precursor and promoter of NAD (nicotinamide adenine dinucleotide). Exogenous administration of NMN can increase the level of NAD in vivo, thereby alleviating aging-related bone loss and resulting osteoporosis.

NMN also plays a significant role in maintaining stem cell activity in bone homeostasis.

Whether NMN can promote the proliferation of bone stem cells and accelerate fracture healing is still unclear.

In this work, we established a mouse model of femoral transverse fracture and evaluated the short - and long-term effects of exogenous NMN administration on fracture healing. It was found that increased NAD content in callus promoted the formation of cartilage callus and accelerated the transformation of cartilage callus into scleroid callus.

The growth of cartilage callus can be attributed to NMN promoting the expansion of multiple bone stem cells at the injury site by up-regulating Notch signaling pathway.

The effect of NMN on promoting stem cell proliferation and migration has been verified in vitro.

The proliferation potential of stem cells benefiting from NMN in callus was significantly impaired after removal of macrophages by clodronate liposomes, suggesting that macrophage-stem cell interaction is critical in callus formation.

This study provides new ideas for the potential application of NAD intermediates (such as NMN, NR, etc.) in bone injury repair.

Tag: NMN

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