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暂时的受体潜能通道TRPM4有利于氧化低密度脂蛋白诱导的冠状动脉内皮细胞功能障碍,通过涉及铁代谢的机制

Fengxiang Ye¹, Dongtao Liu¹, Junjie Zhang²

¹Cardiology Department, Xuzhou Renci Hospital, Xuzhou, Jiangsu 221000, China.

|December 16, 2023

概括

暂时受体潜在通道TRPM4 (TRPM4) 加快动脉样硬化进展. 在内皮细胞中抑制TRPM4可减少炎症和氧化应激,可能通过影响铁含量和铁.

科学领域:

心血管生物学心血管生物学
内皮细胞生物学内皮细胞生物学
动脉样硬化研究动脉样硬化研究

背景情况:

动脉样硬化 (AS) 的进展与内皮损伤有关.
暂时受体潜能通道TRPM4 (TRPM4) 在内皮细胞中表达,并由激活.
需要阐明TRPM4在AS病变发生中的作用.

研究的目的:

研究TRPM4在动脉样硬化中的作用.
探索TRPM4参与内皮功能障碍的潜在机制.

主要方法:

人类冠状动脉内皮细胞 (HCAEC) 用氧化低密度脂蛋白 (ox-LDL) 进行治疗,以模拟AS.
进行了TRPM4的淘汰,以评估其影响.
评估了细胞炎症,氧化应激,内皮功能,脂质过氧化,细胞内铁和铁的标志物.
细胞还用铁灭诱导剂erastin进行了治疗.

主要成果:

在暴露于ox-LDL的HCAEC中,TRPM4表达增加.
TRPM4敲击减轻了ox-LDL诱导的炎症,氧化应激,脂质过氧化,并保持了内皮功能.
埃拉斯治疗逆转了TRPM4敲击的保护作用,加剧了细胞损伤.
TRPM4的淘汰影响了细胞内铁水平和与铁亡相关的蛋白质.

结论:

TRPM4的抗击作用可以防止ox-LDL诱导的内皮炎症,氧化应激和功能障碍.
TRPM4可能通过涉及细胞内铁和ferroptosis的机制促进AS进展.

关键词:

冠心病是一种冠心病.铁性化 (ferroptosis) 是一种在 HCAECEC 中.氧-LDL是一种LDL.TRPM4 TRPM4 在线播放

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