破骨细胞
组织蛋白酶K
骨吸收
骨质疏松症
体内
兰克尔
NF-κB
癌症研究
化学
骨重建
信号转导
细胞生物学
体外
药理学
激活剂(遗传学)
医学
内科学
生物
生物化学
受体
生物技术
作者
Chunchun Xue,Huan Luo,Libo Wang,Qing Deng,Wenyun Kui,Weiwei Da,Lin Chen,Shuang Liu,Y. Xue,Jiafan Yang,Lingxing Li,Wenlan Du,Qi Shi,Xiaofeng Li
标识
DOI:10.3389/fendo.2023.1234563
摘要
. Importantly, AC can regulate osteoclast ferroptosis by suppressing Gpx4 and upregulating Acsl4, which is achieved through inhibition of the phosphorylation of I-κB and p65 in the NF-κB signaling pathway. These findings suggest that AC is a potential therapeutic option for managing OP by suppressing NF-κB signaling-mediated osteoclast ferroptosis and formation.
科研通智能强力驱动
Strongly Powered by AbleSci AI