Volume 4,Issue 4
Osteoporosis (OP) is a metabolic bone disease characterized by decreased bone mineral density and microstructural deterioration, leading to an elevated risk of fragility fractures. Bone remodeling relies on the dynamic balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption. Exosomes, as key mediators of intercellular communication, regulate the differentiation and function of bone marrow mesenchymal stem cells (BMSCs), osteoblasts, and osteoclasts by delivering bioactive molecules (e.g., miRNAs), thereby playing a pivotal role in OP pathogenesis. Recent studies have revealed that the PI3K/Akt signaling pathway not only serves as a central regulator of BMSC osteogenic differentiation but also synergizes with exosomes to promote bone formation by activating downstream targets (e.g., RUNX2, BMP2). This review systematically summarizes the synergistic mechanisms of exosomes and the PI3K/Akt pathway in osteogenesis, focusing on how specific miRNAs (e.g., miR-19a-3p, miR-935) modulate key molecules (e.g., PTEN, STAT1) to restore bone metabolic homeostasis. These findings provide novel insights into the molecular mechanisms of OP and lay a theoretical foundation for developing targeted therapeutic strategies.