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孕期暴露于PM_2.5通过ANGPTL4-介导的线粒体代谢功能障碍影响了心脏发育

Jianong Lv¹, Ruiyang Ding¹, Chen Liang¹

¹Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, China; Laboratory for Clinical Medicine, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environment and Aging, Capital Medical University, Beijing 100069, China.

Journal of advanced research

|November 17, 2025

概括

母亲接触细颗粒物 (PM2.5) 可以通过损害心脏发育导致先天性心脏缺陷. 这项研究确定了ANGPTL4介导的线粒体功能障碍作为关键机制,为预防提供了洞察力.

科学领域:

环境健康环境健康
心血管生物学心血管生物学
线粒体医学线粒体医学

背景情况:

流行病学研究将母亲接触细颗粒物 (PM2.5) 与先天性心脏缺陷 (CHD) 联系起来.
导致PM2.5引起的心脏异常的精确分子机制在很大程度上是未知的.
了解这些机制对于制定针对环境病原体的预防策略至关重要.

研究的目的:

调查PM2.5暴露对胎儿心脏发育的影响.
为了阐明PM2.5引起的心脏缺陷所涉及的分子途径.
确定PM2.5相关心血管形的潜在生物标志物.

主要方法:

对人类带血清进行潜在生物标志物的分析 (ANGPTL4,SIRT3,D2-HG).
在子宫内暴露于PM2.5的小鼠,以评估心脏发育和线粒体功能.
基因操纵 (ANGPTL4淘汰),以评估保护作用.
在体外研究探索ANGPTL4,SIRT3,LONP1和D2HGDH之间的分子相互作用.

主要成果:

在子宫内暴露于PM2.5导致左心室壁厚度增加,并导致后代小鼠的线粒体功能障碍.
ANGPTL4,SIRT3和D2-HG被确定为PM2.5相关心脏缺陷的潜在生物标志物.
ANGPTL4淘汰赛减弱了PM2.5引起的心脏病理.
暴露于PM2.5会破坏ANGPTL4-SIRT3-LONP1轴,通过D2HGDH损害线粒体质量控制和能量代谢.

结论:

暴露于PM2.5会通过ANGPTL4介导的线粒体功能障碍损害心脏发育.
这项研究提供了环境污染物和先天性心脏缺陷之间的机制联系.
这些发现表明,PM2.5相关的先天缺陷的预防和治疗有新的目标.

关键词:

ANGPTL4 在线观看空气污染大气污染心脏发育的心脏发育微细颗粒物 (PM2.5)) 是一种微细颗粒物.线粒体能量代谢的能量代谢

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