股骨头坏死中骨微血管内皮细胞对氧化应激性损伤的修复机制
Repair mechanisms of bone microvascular endothelial cells against oxidative stress injury in osteonecrosis of the femoral head
张兆坤 1赵俊杰 1王玺玉 1黄鹏飞 1赵海燕1
作者信息
- 1. 兰州大学第一临床医学院,兰州 730000;兰州大学第一医院骨科,兰州 730000
- 折叠
摘要
激素性股骨头坏死是临床患者应用糖皮质激素治疗过程中的一种严重副作用.尽管糖皮质激素诱导的股骨头坏死的确切机制尚未完全明确,但既往研究显示其过程可能涉及骨相关细胞(骨髓间充质干细胞、成骨细胞、破骨细胞等)病理生理的变化,最终导致骨修复障碍.近年来,随着血管假说的提出,发现骨微血管内皮细胞(BMECs)以成骨-成血管偶联方式在骨形成和骨吸收中发挥重要作用.糖皮质激素的大量应用会使BMECs通过氧化应激的病理形式最终导致细胞的凋亡、衰老和过度自噬等病理生理变化,造成骨微血管网的损伤,从而影响股骨头局部修复.本文旨在通过探讨BMECs在氧化应激损伤下的作用机制,揭示其如何预防和抑制糖皮质激素诱导的股骨头坏死,为深化股骨头坏死的研究提供重要参考与理论依据.
Abstract
Glucocorticoid(GC)-induced osteonecrosis of the femoral head(ONFH)is a severe adverse event in patients receiving GC therapy.While the precise mechanisms of GC-induced ONFH remains unclear,previous studies suggest that it may involve pathophysiological changes in bone-related cells,such as bone marrow mesenchymal stem cells,osteoblasts,and osteoclasts,ultimately leading to bone repair disorders.In recent years,the introduction of the vascular hypothesis has highlighted the significant role of bone microvascular endothelial cells(BMECs)in bone formation and resorption through an osteogenic-angiogenic coupling mechanism.The extensive application of GCs can lead to oxidative stress in BMECs,ultimately resulting in pathophysiological changes such as apoptosis,senescence,and excessive autophagy,which disrupt the bone microvascular network and hinder local repair of the femoral head.This study aimed to discuss the mechanisms by which oxidative stress-induced damage to BMECs can prevent and halt GC-induced ONFH,providing insights and references for further research on ONFH.
关键词
股骨头坏死/糖皮质激素/骨内皮细胞/成骨-成血管偶联Key words
Osteonecrosis of the Femoral Head/Glucocorticoids/Bone Endothelial Cells/Pathophysiology/Osteogenic-Angiogenic Coupling引用本文复制引用
基金项目
国家自然科学基金(82060394)
兰州市人才创新创业项目(2020-RC-45)
兰州大学第一医院院内基金(ldyyyn2022-73)
出版年
2024
NETL
NSTL
万方数据