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在先进的动脉样硬化期间,HMOX1-LDHB相互作用通过诱导发泡性巨细胞中的线粒体功能障碍来促进铁亡

Xiang Peng¹, Bin Sun², Chaohui Tang¹

¹Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Heilongjiang Provincial Key Laboratory of Panvascular Disease, Harbin 150086, China; The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin 150081, China.

Developmental cell

|December 28, 2024

概括

由铁的积累和线粒体功能障碍驱动的泡性巨细胞铁,加速动脉样硬化. 用MitoTEMPO或LONP1抑制剂准这个过程为心血管疾病提供了新的治疗策略.

科学领域:

心血管生物学心血管生物学
细胞的新陈代谢
免疫病理学免疫病理学

背景情况:

晚期动脉样硬化是急性心血管事件的基础,尽管治疗,风险仍然存在.
泡性巨细胞死亡显著导致动脉样硬化斑块的进展,但机制尚不清楚.
巨细胞中铁的积累与晚期动脉样硬化有关.

研究的目的:

阐明推动发达动脉样硬化中的泡性巨体铁亡的细胞和分子机制.
为了确定缓解动脉样硬化进展的潜在治疗点.

主要方法:

大量和单细胞RNA测序用于分析动脉样硬化中的巨细胞群.
在泡状巨中评估氧化酸化 (OXPHOS) 的代谢分析.
研究血氧酶1 (HMOX1) - 乳酸脱酶B (LDHB) 和伦酶1 (LONP1) 在线粒体功能障碍中的作用.
在动脉样硬化模型中使用MitoTEMPO和 bortezomib的体内研究.

主要成果:

大量的铁积累促进泡性巨细胞的铁,特别是在TREM2低的巨细胞中.
TREM2低泡性巨细胞表现出低的OXPHOS,增加了ferroptosis的敏感性.
上调的HMOX1-LDHB相互作用促进了LONP1-介导的TFAM降解,导致线粒体功能障碍和铁亡.
米托波和博特佐米布治疗恢复了线粒体平衡,减少了动脉样硬化.

结论:

由铁过载和涉及LONP1的特定分子途径介导的泡性巨细胞铁亡是晚期动脉样硬化的关键驱动因素.
针对泡性巨细胞中的线粒体功能障碍和铁亡,为动脉样硬化提供了一个有希望的治疗途径.

关键词:

LDHBB LDHB LDHB LDHB LDHB LDHB LDHB LDHB LDHB TREM2 (低) 泡性巨细胞晚期动脉样硬化症的发生铁性化 (ferroptosis) 是一种线粒体功能障碍线粒体功能障碍

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