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H3K14la通过促进SLC40A1 / 转林介导的铁灭症来驱动败血症诱导的ARDS中的内皮功能障碍

Fangchen Gong¹, Xiangtao Zheng¹, Wen Xu²

¹Department of Emergency Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.

|January 17, 2025

概括

败血症会导致乳酸的积累,导致肺细胞中的组素乳酸化. 这一过程,特别是H3K14乳化,驱动细胞功能障碍和肺损伤在败血症引起的急性呼吸困扰综合征.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
病理生理学病理生理学

背景情况:

肺内皮细胞 (EC) 的激活是急性呼吸困扰综合征 (ARDS) 的核心.
败血症诱导的葡萄糖溶解会增加乳酸,导致蛋白质氨酸乳化 (Kla),但其在ARDS中EC功能障碍中的作用尚不清楚.

研究的目的:

为了研究蛋白质乳糖化,特别是基因素H3 lysine 14乳糖化 (H3K14la) 在败血症诱导的ARDS期间内皮细胞功能障碍中的作用.
为了确定链接糖解,乳酸和肺损伤在败血症的分子机制.

主要方法:

在败血症小鼠肺组织中进行了整合性乳和蛋白质组分析.
切割和标记分析以确定ECs中的H3K14la转录目标.
评估糖解抑制对H3K14la和EC激活的影响.

主要成果:

败血症小鼠在肺部EC中显示乳酸和H3K14la的增加.
抑制糖解降低了H3K14la和EC激活,证实了糖解-乳糖化联系.
在铁灭基因 (TFRC,SLC40A1) 的促进者中发现了H3K14la,有助于EC激活和肺损伤.

结论:

乳酸依赖的H3K14乳化调节EC铁,在败血症引起的肺损伤中促进血管功能障碍.
针对糖解/H3K14la/ferroptosis路径为与败血症相关的ARDS提供了潜在的治疗策略.

关键词:

内皮质功能障碍在内皮质功能障碍铁性化 (ferroptosis) 是一种乳化乳化乳化肺部受伤的原因是肺部损伤.这是一种血症.

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