纺神星
炎症
外周血单个核细胞
疾病
机制(生物学)
外周血
生长因子
成纤维细胞生长因子23
成纤维细胞生长因子
外围设备
医学
成纤维细胞
阿尔茨海默病
癌症研究
内科学
免疫学
生物
细胞生物学
病理
细胞培养
遗传学
受体
钙
体外
哲学
肾
认识论
甲状旁腺激素
作者
Baoshan Li,Min Zhou,Jing Peng,Qiao Yang,Jingxin Chu,Ruoqing Li,Yi Jiang
标识
DOI:10.1080/08820139.2021.1970180
摘要
Alzheimer's disease (AD) is a prevalent type of dementia and threatens the health of most elderly people and poses a huge burden to families and society. The fibroblast growth factor 23 (FGF23)/α-Klotho axis is associated with multiple aging-related diseases. Hence, this study explored the mechanism of the FGF23/α-Klotho axis in AD. FGF23/α-Klotho protein contents and levels of inflammatory cytokines in AD patients were measured, and the correlation between FGF23/α-Klotho protein contents and inflammatory cytokines was analyzed. FGF23 and α-Klotho expressions were blocked in peripheral blood mononuclear cells (PBMCs) in AD patients (AD-PBMCs) to assess the effects on cell inflammation and the Wnt/β-catenin pathway activation. The Wnt/β-catenin pathway was inhibited to evaluate cell inflammation. Combined treatments of the cells were conducted to verify the role of the FGF23/α-Klotho axis and the Wnt/β-catenin pathway in inflammation in AD-PBMCs. Increased FGF23 protein concentration and reduced α-Klotho protein concentration were observed in AD patients and correlated with inflammatory cytokine levels. FGF23 inhibition or α-Klotho overexpression reduced the production of inflammatory cytokines and activated the Wnt/β-catenin pathway in AD-PBMCs. Blocking the Wnt/β-catenin pathway increased inflammatory cytokine production in AD-PBMCs and annulled the effects of the FGF23/α-Klotho axis on AD-induced cell inflammation. We concluded that the FGF23/α-Klotho axis can regulate the AD-induced cell inflammation through the Wnt/β-catenin pathway.
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