氧化应激在激素性股骨头坏死发病机制中的研究进展

Research Progress on Oxidative Stress in the Pathogenesis of Steroid-Induced Osteonecrosis of the Femoral Head

大量研究表明,氧化应激参与了激素性股骨头坏死(SONFH)的发病过程。活性氧(ROS)在维持细胞正常功能中起着至关重要的作用,但在氧化应激状态下,过量的ROS会导致多种细胞损伤,引起疾病发生。氧化应激引起血管内皮损伤、间充质干细胞功能障碍、成骨细胞及骨细胞凋亡、破骨细胞过度活化,导致SONFH发生。本文就氧化应激在SONFH发病机制中的研究进展作一综述。

Considerable evidence suggests that oxidative stress is involved in the pathogenesis of steroid- induced osteonecrosis of the femoral head (SONFH). Reactive oxygen species (ROS) play a crucial role in maintaining normal cellular function, but excessive ROS under oxidative stress conditions can lead to various forms of cellular damage, contributing to disease onset. Oxidative stress induces endothelial injury, dysfunction of mesenchymal stem cells, apoptosis of osteoblasts and osteocytes, and excessive activation of osteoclasts, resulting in the occurrence of SONFH. This review provides an overview of the research progress on oxidative stress in the pathogenesis of SONFH.