氧化应激
细胞凋亡
弧(几何)
线粒体
细胞生物学
化学
病态的
氧化损伤
衰老
β淀粉样蛋白
氧化磷酸化
内分泌学
癌症研究
内科学
生物
医学
阿尔茨海默病
疾病
生物化学
几何学
数学
作者
Peimin Lin,Jie Xu,Fan Yang,Dan Li,Rong Zhang,Yongxiang Jiang,Tianyu Zheng
标识
DOI:10.1096/fj.202301281rr
摘要
Abstract Recently, amyloid‐β oligomers (AβOs) have been studied as the primary pathogenic substances in Alzheimer's disease (AD). Our previous study revealed that the Aβ expression level is closely related to ARC progression. Here, we demonstrated that the accumulation of AβOs in the lens epithelium of age‐related cataract (ARC) patients increased during ARC progression and that this alteration was consistent with the changes in mitochondrial function, oxidative stress, and cellular apoptosis. In vitro, human lens epithelial cells (HLECs) treated with AβOs exhibited Ca 2+ dyshomeostasis, impaired mitochondrial function, elevated oxidative stress levels, and increased apoptosis. Moreover, the proapoptotic effect of AβOs was alleviated after the uptake of mitochondrial Ca 2+ was inhibited. These results establish that AβOs may promote HLEC apoptosis by inducing mitochondrial Ca 2+ overload, thus preliminarily revealing the possible association between the accumulation of AβOs and other pathological processes in ARC.
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