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外体miR-27a-5p通过向USF2/FUT8轴来抑制因多硫酸盐引起的心脏功能障碍

Kun Xiao¹, Jiaojiao Hao², Nan Wang¹

¹Department of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, Branch of National Clinical Research Center for Kidney Diseases, Dalian, China; Graduate School of Dalian Medical University, Dalian, China.

Free radical biology & medicine

|September 24, 2025

概括

在血液透析患者中,酸硫酸 (IS) 通过外体细胞核化 (CF) 驱动尿路性心肌病 (UCM). 抑制CF通过降低ARG2和活性氧物种 (ROS) 的调节来减少心脏损伤.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
毒理学毒理学毒理学

背景情况:

尿路性心肌病变 (UCM) 是血液透析患者的主要死亡原因.
硫酸 (IS),一个关键的尿素毒素,促进心脏缩和亡.
心脏微血管内皮细胞 (CMECs) 和心肌细胞 (CMs) 之间的外介导交叉声有助于UCM的进展.

研究的目的:

调查核心化 (CF) 修饰在IS诱导的CMEC衍生外体 (IS-Exos) 中的作用及其对CM损伤的影响.
阐明关联IS,CF和UCM的潜在分子机制.

主要方法:

利用IS诱导心脏损伤的微流体芯片模型可视化外体转移并评估CM损伤.
通过使用淘汰赛小鼠和siRNA在暴露于IS-Exos的CM中抑制α1,6-fucosyltransferase (FUT8) 的效果.
分析了miR-27a-5p,CD44,EGFR,ARG2和活性氧物种 (ROS) 在致病级联中的作用.

主要成果:

在血液透析患者中,血清IS和FUT8水平升高与心脏损伤严重程度相关.
在CM中,IS-Exos诱导了线粒体功能障碍,高和亡,CF发挥了关键作用.
抑制FUT8降低了ARG2表达,降低了ROS,并改善了心脏缩和亡.
在IS-Exos中观察到miR-27a-5p的下调;miR-27a-5p补充向USF2,减少FUT8和ARG2,从而减轻心脏损伤.

结论:

核心 IS-Exos 的 fucosylation 是在 UCM 中IS 诱导的心脏损伤的关键调解者.
针对CF修饰,可能通过miR-27a-5p/USF2/FUT8/ARG2轴,为UCM提供了一个有前途的治疗策略.

关键词:

核心的福克苏化.印度硫酸盐印度酸盐细胞内通信细胞内通信有反应性氧物种的反应性氧物种.尿路性心肌病变性是什么微型RNA-27a-5pp是什么意思

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