[Exercise improves osteoporosis through bone-fat crosstalk]

Osteoporosis (OP) is a prevalent systemic metabolic bone disease characterized by reduced bone mass and compromised bone microstructure. Recent studies have demonstrated that the occurrence of OP is closely related to the imbalance of bone and lipid metabolism. Bone and lipid can communicate and influence each other by secreting bone-derived factors or adipokines. This kind of crosstalk is crucial for maintaining the equilibrium between bone and fat. Meanwhile, multiple signaling pathways such as Wnt/β-catenin, bone morphogenetic protein (BMP), mitogen-activated protein kinase (MAPK), peroxisome proliferator-activated receptor γ (PPARγ), Notch, Hedgehog, and PI3K/Akt pathways can also regulate bone-fat crosstalk. In addition, in the bone marrow microenvironment, bone marrow mesenchymal stem cells (BMSCs), osteoblasts, osteoclasts, osteocytes, and adipocytes also have close interactions, jointly maintaining bone-lipid metabolic balance. Exercise, as a non-invasive intervention method, can regulate bone tissue, adipose tissue, and bone marrow adipose tissue in multiple aspects and shows great potential in improving OP. Although the effect of exercise on bone-lipid metabolism has been widely confirmed, its specific molecular mechanism and its role in bone-fat crosstalk still need further exploration. In light of this, based on the review of research progress related to bone-fat crosstalk, this article summarizes the effects of exercise on this crosstalk and its underlying mechanism in improving OP, providing theoretical basis for the prevention and treatment of OP through exercise.