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在脑血管动脉样硬化中,N6-甲基氨酸 (m6A) 阅读器YTHDF2加速内皮细胞铁亡

Jia Li¹, Changlin Zou², Zhiming Zhang¹

¹Department of Surgery, Tianjin Nankai Hospital, Tianjin Medical University, No. 6 Changjiang Road, Tianjin, 300100, China.

Molecular and cellular biochemistry

|October 4, 2023

概括

YTHDF2加速血管内皮细胞中的铁亡,这是脑血管动脉样硬化的关键过程. 这一发现增强了对疾病的理解.

科学领域:

生物医学科学生物医学科学
分子生物学分子生物学
心血管研究研究心血管研究

背景情况:

脑血管疾病,包括动脉样硬化,导致全球高死亡率和残疾.
内皮细胞损伤是动脉样硬化的主要驱动因素,是脑血管疾病的主要原因.
铁,一种涉及铁和脂质过氧化的编程细胞死亡形式,与动脉样硬化进展有关.

研究的目的:

在动脉样硬化期间研究YTHDF2在血管内皮细胞中的作用和机制.
阐明YTHDF2在动脉样硬化背景下如何影响内皮细胞增殖和铁亡.

主要方法:

使用了用氧化低密度脂蛋白 (ox-LDL) 治疗的人类脉内皮细胞 (HUVEC).
进行了功能增益和功能丧失测定,以评估YTHDF2对细胞增殖和铁亡的影响.
在分析中使用,以确定SLC7A11 mRNA和YTHDF2结合相互作用上的潜在m6A修饰位.

主要成果:

在ox-LDL治疗的HUVEC中,YTHDF2表达被上调.
过度表达YTHDF2抑制了HUVEC的扩散,并促进了铁亡.
沉默YTHDF2增强了HUVEC的扩散,并减少了铁亡.
YTHDF2以m6A依赖的方式与SLC7A11mRNA结合,促进其降解并降低稳定性.

结论:

YTHDF2加速内皮细胞中的铁亡,导致脑血管动脉样硬化.
这些发现提供了关于脑血管疾病病理机制的见解.
向YTHDF2可能为动脉样硬化提供治疗策略.

关键词:

动脉样硬化是一种动脉样硬化.铁化是铁化的一种.这是一种N6-甲基氨酸.在 SLC7A1111 中.这就是YTHDF2的原因.

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