目前对骨性关节炎的治疗主要为抗炎止痛、矫正畸形等对症治疗,对因治疗方案尚欠缺.软骨细胞的程序性死亡和软骨退化与骨性关节炎的发生发展密切相关.近年来,铁死亡作为新发现的细胞程序性死亡广受关注.研究者针对软骨细胞铁死亡,对谷胱甘肽过氧化物酶4(glutathione peroxidase 4,GPX4)铁死亡抵抗途径、铁代谢途径、脂质过氧化、核因子E2相关因子2(nuclear factor erythroid-2 related factor2,Nrf-2)/一氧化碳氧化酶1(heme oxygenase-1,HO-1)通路、有丝分裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)/核因子κB(nuclear factor-KB,NF-κB)通路等相互联系的铁死亡机制进行了深入的研究.通过干预软骨细胞铁死亡相关的信号通路和分子,可能有望减缓软骨退化的进程,甚至为骨性关节炎的治疗提供新的治疗靶点.
Abstract
Currently,the treatment of osteoarthritis primarily involves symptomatic management,such as anti-inflammatory pain relief and correction of deformities,with lacking causative treatment strategies.Research has revealed a close association between the programmed cell death of chondrocytes and the degeneration of cartilage in the development of osteoarthritis.Ferroptosis,a newly discovered form of programmed cell death,has garnered significant attention recently.Researchers have conducted in-depth investigations into the ferroptosis mechanisms,including the GPX4 ferroptosis resistance pathway,iron metabolism pathway,lipid peroxidation,Nrf-2/HO-1 pathway,NF-κB/MAPK pathway,and their interrelated aspects concerning chondrocytes ferroptosis.The comprehensive study of these related pathways provides a new direction for the treatment of osteoarthritis.By intervening in the signaling pathways and molecules associated with chondrocyte ferroptosis,there is potential to slow down the process of cartilage degradation and even identify novel therapeutic targets for the management of osteoarthritis.
维普
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