骨质疏松,严重的健康疾病之一,涉及骨质流失,骨密度减少,骨微结构的退化,伴随着骨骼脆弱的趋势和骨折的倾向。全世界有超过2亿人患有骨质疏松症,到2025年,治疗骨质疏松性骨折的费用预计将达到至少250亿美元。骨质疏松的产生和发展受遗传因素和TGF-β等调节因子的调控,BMP,和FGF通过多种途径,包括Wnt信号通路,Notch信号通路,和MAPK信号通路。其中,Wnt信号通路是最重要的信号通路之一。它不仅参与骨骼发育和代谢,还参与软骨细胞的分化和增殖,间充质干细胞,破骨细胞,和成骨细胞。Dkk-1和SOST是Wnt抑制蛋白,可以抑制经典Wnt信号通路的激活,阻断成骨细胞的增殖和分化。因此,它们可以作为治疗骨质疏松症的潜在靶点。在这次审查中,我们分析了Wnt蛋白的作用机制,β-连环蛋白,和信号分子在信号转导过程中的作用,并总结了Wnt信号通路与骨相关细胞的关系。我们希望引起人们对Wnt信号通路在骨质疏松症中的作用的关注,并为骨质疏松症的诊断和治疗提供新的视角和方法。
Osteoporosis, one of the serious health diseases, involves bone mass loss, bone density diminishing, and degeneration of bone microstructure, which is accompanied by a tendency toward bone fragility and a predisposition to fracture. More than 200 million people worldwide suffer from osteoporosis, and the cost of treating osteoporotic fractures is expected to reach at least $25 billion by 2025. The generation and development of osteoporosis are regulated by genetic factors and regulatory factors such as TGF-β, BMP, and FGF through multiple pathways, including the Wnt signaling pathway, the Notch signaling pathway, and the MAPK signaling pathway. Among them, the Wnt signaling pathway is one of the most important pathways. It is not only involved in bone development and metabolism but also in the differentiation and proliferation of chondrocytes, mesenchymal stem cells, osteoclasts, and osteoblasts. Dkk-1 and SOST are Wnt inhibitory proteins that can inhibit the activation of the canonical Wnt signaling pathway and block the proliferation and differentiation of osteoblasts. Therefore, they may serve as potential targets for the treatment of osteoporosis. In this review, we analyzed the mechanisms of Wnt proteins, β-catenin, and signaling molecules in the process of signal transduction and summarized the relationship between the Wnt signaling pathway and bone-related cells. We hope to attract attention to the role of the Wnt signaling pathway in osteoporosis and offer new perspectives and approaches to making a diagnosis and giving treatment for osteoporosis.