兰克尔
破骨细胞
骨质疏松症
蛋白激酶B
骨吸收
PI3K/AKT/mTOR通路
内分泌学
内科学
肿瘤坏死因子α
化学
医学
癌症研究
NF-κB
信号转导
炎症
受体
生物化学
激活剂(遗传学)
作者
Li Zha,Li He,Yijian Liang,Hui Qin,Bin Yu,Lin‐Li Chang,Li Xue
标识
DOI:10.1016/j.biopha.2018.03.080
摘要
Previous studies showed that inflammatory cytokines promote osteoclast formation, characterized by the function of bone resorption. However, it remains unclear whether inflammatory factors contribute to osteoporosis syndrome in postmenopausal women. Here, we found that postmenopausal women with osteoporosis (PO) had increased levels of TNF-α, compared with those without osteoporosis. TNF-α is highly correlated with the RANK and estrogen levels in PO patients. in vitro, TNF-α synergistically promotes RANKL-induced osteoclast formation by activation of NF-κB and PI3K/Akt signaling. Moreover, inhibition of PI3K/Akt totally blocked the synergistic effects of TNF-α on NF-κB activation as well as osteoclast formation. Together, these results demonstrate that TNF-α synergistically promotes RANKL-induced osteoclasts formation through activation of PI3K/Akt signaling, which ultimately contributes to osteoporosis syndrome in postmenopausal women.
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