Repair mechanisms of bone microvascular endothelial cells against oxidative stress injury in osteonecrosis of the femoral head
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.
Osteonecrosis of the Femoral HeadGlucocorticoidsBone Endothelial CellsPathophysiologyOsteogenic-Angiogenic Coupling
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