Mechanism by which vascular endothelial growth factor A targets regulation of angiogenesis in the treatment of steroid-induced osteonecrosis of the femoral head
- VernacularTitle:血管内皮生长因子A靶向调控血管化治疗激素性股骨头坏死的机制
- Author:
Zhengye WANG
1
;
Wanlin LIU
1
;
Zhenqun ZHAO
1
Author Information
- Publication Type:Journal Article
- Keywords: vascular endothelial growth factor A; steroid-induced osteonecrosis of the femoral head; phosphatidylinositol 3 kinase; serine/threonine protein kinase B; apoptosis; extracellular vesicles; engineered tissue construction
- From: Chinese Journal of Tissue Engineering Research 2026;30(3):671-679
- CountryChina
- Language:Chinese
- Abstract: BACKGROUND:Steroid-induced osteonecrosis of the femoral head(SANFH)is a severe orthopedic disease characterized by interruption of the blood supply to the femoral head and necrosis of subchondral bone,leading to joint dysfunction.Long-term use of glucocorticoids is the main cause of SANFH,and its pathogenesis involves multiple factors,including intravascular coagulation and osteocyte apoptosis.Vascular endothelial growth factor A(VEGF-A),as a key angiogenic factor,has potential value in the treatment of SANFH.OBJECTIVE:To summarize the mechanisms of action of VEGF-A in SANFH,including its progress in promoting angiogenesis,anti-apoptosis,and lipid metabolism regulation,and to discuss the prospects for clinical application of VEGF-A targeted therapy.METHODS:Literature related to VEGF-A targeted regulation of angiogenesis in the treatment of SANFH was identified through searches of PubMed,Web of Science,CNKI,and WanFang databases from database inception to November 2024.After quality assessment,71 articles were selected,data were extracted by independent researchers,and disagreements were resolved through group discussions.RESULTS AND CONCLUSION:(1)VEGF-A binds to its receptors VEGFR-1 and VEGFR-2,activating downstream signaling pathways that promote the proliferation,migration,and angiogenesis of endothelial cells.Therefore,it can promote the formation of collateral circulation and improve blood supply to the area of bone necrosis.(2)Reduced expression of VEGF-A may lead to a decrease in the number of blood vessels within bone tissue,exacerbating the ischemic state of the femoral head.Furthermore,VEGF-A has anti-apoptotic effects and reduce apoptosis in osteocytes and bone marrow cells,thus protecting bone tissue.(3)The role of VEGF-A in regulating lipid metabolism and inflammatory responses,as well as promoting the osteogenic differentiation of bone marrow mesenchymal stem cells,provides a new perspective for the treatment of SANFH.(4)The development of VEGF-A protein delivery systems,such as lipid nanoparticles and exosome-based delivery systems,offers new possibilities for the clinical application of VEGF-A.(5)The research progress of VEGF-A in SANFH treatment has laid a solid foundation for the development of new treatment strategies and has opened up new avenues for future research directions and clinical applications.(6)With further clarification of the mechanisms of action of VEGF-A and continuous advancements in delivery technologies,more effective treatments will be provided for SANFH patients,improving their prognosis.
