下调和上调
脂质代谢
胆固醇
平衡
小RNA
载脂蛋白B
人口
生物标志物
内分泌学
内科学
转录组
生物
表观遗传学
调解人
载脂蛋白E
泡沫电池
细胞生物学
细胞内
化学
小窝
代谢组学
微泡
ABCA1
细胞
镉暴露
流出
基因表达调控
药理学
新陈代谢
载脂蛋白A1
氧化应激
动脉硬化
生物化学
微泡
PCSK9
作者
Tian Wang,Ziquan Lv,Xuejun Fu,Yanwei Zhang,Dongju Zou,Jiaxin Chen,Ziyang Zou,Jinling Liu,Chao Wang,Y. Xiong,Guimiao Lin,Yuewei Liu,Peiyi Liu,Jinquan Cheng,Suli Huang
标识
DOI:10.1021/acs.est.5c07383
摘要
, respectively, thereby promoting intracellular lipid accumulation. In a case-control population (494 IS patients and 494 controls), plasma miR-30d-5p levels were positively associated with Cd exposure and partially mediated the Cd-stroke association, accounting for 16.4% of the total effect. Moreover, miR-30d-5p significantly improved the discrimination and reclassification of IS patients beyond the traditional risk factors. In summary, our findings reveal that Cd induces atherosclerosis by disrupting cholesterol homeostasis and modulating miRNA-regulated pathways with plasma miR-30d-5p serving as a potential biomarker and mediator for Cd-related ischemic stroke. Further perspective investigations are warranted to validate our findings.
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