Osteoporosis (OP) is a complex systemic disease characterized by a loss of bone density, leading to bone fragility and an increase risk of fractures of the hip, spine and wrist. The clinical therapeutic effect is still far from satisfactory. Thus, further studies are urgently needed to explore the pathogenesis of OP. In this study, our aim is to explore the underlying molecular mechanism of lncRNA H19/miR-29a-3p axis for regulating of inflammation, proliferation and apoptosis in OP. The expression of lncRNA H19 was significantly upregulated in OP samples compared with the health control. Subsequently, we found that miR-29a-3p is the target of lncRNA H19 in OP. Furthermore, the knockdown of lncRNA H19 was validated to promote the expression of pro-inflammatory mediators, repress cell proliferation and inhibit cell apoptosis in vitro. Moreover, the modulating effects of lncRNA-H19 on the expressions of pro-inflammatory mediators, cell proliferation and apoptosis in vitro were diminished after co-transfecting with miR-29a-3p inhibitor and siRNA-H19. Thus, we concluded that lncRNA H19/miR-29a-3p axis was involved in the development of OP. This study might provide a better understanding of OP development and a potential therapeutic target for OP intervention.

骨质疏松症（OP）是一种复杂的全身性疾病，其特征是骨骼密度降低，导致骨骼脆弱，并增加了髋部，脊柱和腕部骨折的风险。临床治疗效果仍远未令人满意。因此，迫切需要进一步研究以探讨OP的发病机理。在这项研究中，我们的目的是探索lncRNA H19 / miR-29a-3p轴调控OP中炎症，增殖和凋亡的潜在分子机制。与健康对照相比，OP样品中lncRNA H19的表达显着上调。随后，我们发现miR-29a-3p是OP中lncRNA H19的靶标。此外，已证实敲低lncRNA H19可促进促炎性介质的表达，抑制细胞增殖并抑制细胞凋亡体外。此外，与miR-29a-3p抑制剂和siRNA-H19共转染后，lncRNA-H19对促炎性介质表达，体外细胞增殖和凋亡的调节作用 减弱。因此，我们得出结论，lncRNA H19 / miR-29a-3p轴参与了OP的发展。这项研究可能会更好地了解OP的发展和OP干预的潜在治疗目标。