Osteoporosis is a type of systemic metabolic bone lesion that is prone to bone fractures due to various causes of decreased bone mass and bone density, destruction of bone microarchitecture, and increase of bone fragility. Osteoblasts are the main functional cells that promote bone formation and are the key cells for the development of osteoporosis. Degeneration of osteoblasts and abnormal apoptosis cause bone loss and induce osteoporosis. Therefore, exploring the apoptotic mechanism of osteoblasts is of great significance for the prevention and treatment of osteoporosis. The mitochondrial pathway is the main pathway of osteoblast apoptosis and is a complex process that is formed by the participation of multiple genes and multiple pathways. Therefore, this article reviews the mitochondrial pathway of apoptosis and its many related signaling pathways: PI3k/Akt signaling pathway, MAPK signaling pathway, Ca2+/CaM signaling pathway, and other signaling pathways and factors (Keap1/Nrf2 signaling pathway, PHB, FoxO family, cAMP/CREB). The promotion or inhibition of these signaling pathways in the process of osteoblast apoptosis through the mitochondrial pathway, and some of their interactions in osteoblast apoptosis, are also reviewed. This provide a reliable basis for further exploration of the apoptotic mechanism of osteoblasts and the pathogenesis of osteoporosis, as well as provide some possible targets for a more in-depth study of the safety and efficacy anti-osteoporosis drugs (e.g., Akt, ERK, JNK, p38, Ca2+, PHB, FoxO3a, CREB, Keap1/Nrf2, etc.). |