暴露通过通过miR-30d-5p调节破坏胆固醇恒温促进动脉样硬化
Tian Wang1,2, Ziquan Lv1, Xuejun Fu3
1Shenzhen Center for Disease Control and Prevention, Shenzhen 518055, Guangdong, China.
Environmental science & technology
|November 26, 2025
概括
暴露会促进动脉样硬化和缺血性中风,通过破坏胆固醇代谢和改变microRNAs. 血miR-30d-5p是相关中风的潜在生物标志物.
科学领域:
- 环境健康 环境健康
- 心血管生物学 心血管生物学
- 分子生物学分子生物学
背景情况:
- (Cd) 暴露是动脉样硬化心血管疾病 (ASCVD) 的新兴危险因素,特别是缺血性中风 (IS).
- 微RNAs (miRNAs) 被认为是环境暴露和健康结果之间的调解者,但它们在Cd诱导的IS中的作用尚不清楚.
- 了解这些机制对于制定预防和诊断策略至关重要.
研究的目的:
- 调查miRNAs在Cd诱导的动脉样硬化和缺血性中风中的作用.
- 为了识别特定的miRNA及其向基因,这些基因参与了Cd的亲动脉生成效应.
- 评估血miR-30d-5p作为Cd相关IS的潜在生物标志物.
主要方法:
- 动脉样硬化进展在暴露于Cd和高脂肪饮食的非脂蛋白E缺乏的小鼠中进行了研究.
- 通过脂质资料,基因表达分析 (CD36,ABCA1,NCEH1),转录组和代谢组分析来评估系统和血管胆固醇平衡.
- 使用微阵列进行miRNA表达的分析,随后进行生物信息学分析和qRT-PCR验证.
- 一项病例对照研究 (494名IS患者,494名对照) 检查了血miR-30d-5p,Cd暴露和IS风险之间的关联.
主要成果:
- 在小鼠中,CD暴露加速了动脉样硬化和破坏了胆固醇恒常,由改变的脂质代谢和基因表达证明.
- 鉴定出miR-30d-5p和miR-504-3p是关键调节剂;Cd调高了针对NCEH1的miR-30d-5p,调低了针对CD36的miR-504-3p,促进泡细胞的形成.
- 血miR-30d-5p水平与人类的Cd暴露有积极的关联,并部分调解了Cd-IS关联.
- miR-30d-5p改善了超越传统风险因素的IS预测.
结论:
- 通过破坏胆固醇平衡和调节特定的miRNA通路,Cd暴露会诱导动脉样硬化和缺血性中风.
- 血miR-30d-5p作为Cd相关的缺血性中风的潜在媒介和生物标志物.
- 需要进一步的研究来验证这些发现,并探索治疗干预措施.
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