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Circ_0005699通过准miR-384/ASPH轴加速ox-LDL触发的内皮细胞损伤

Xiaobiao Cao¹, Jun Yang², Lujun He³

¹Department of Internal Medicine, Chinese People Liberation Army (PLA) 93864 Military Hospital, Changji, China.

Cardiovascular toxicology

|July 8, 2024

概括

循环RNAcirc_0005699通过促进内皮细胞损伤加剧动脉样硬化. 针对circ_0005699可能通过调节miR-384/ASPH轴来提供动脉样硬化治疗策略.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
遗传学和基因组学遗传学和基因组学

背景情况:

动脉样硬化 (AS) 是一种复杂的炎症性疾病.
循环RNAs (circRNAs) 在AS病变发生过程中起着重要作用.
了解像circ_0005699这样的特定circRNA对于AS研究至关重要.

研究的目的:

研究circ_0005699在氧化低密度脂蛋白 (ox-LDL) 诱导的人类静脉内皮细胞 (HUVECs) 损伤中的作用和机制.
为了阐明涉及circ_0005699,miR-384和ASPH在AS中的调节途径.

主要方法:

利用牛-LDL诱导HUVEC中的伤害.
评估了AS患者血清和HUVEC中circ_0005699的表达水平.
进行了circ_0005699干扰测定和miR-384结合实验.
研究了miR-384和ASPH之间的相互作用,以及circ_0005699通过miR-384海绵对ASPH的调节作用.

主要成果:

氧-LDL诱导的HUVEC损伤,其特点是降低活力,增殖,血管新生,增加亡,炎症和氧化应激.
在AS患者血清和ox-LDL治疗的HUVEC中,circ_0005699的调节升高.
与circ_0005699的干扰改善了ox-LDL诱导的HUVEC损伤.
Circ_0005699海绵式的miR-384,和miR-384的目标是ASPH. Circ_0005699 通过海绵化进行调节的ASPH表达 miR-384.4.

结论:

环_0005699促进牛LDL诱导的HUVEC损伤.
环_0005699/miR-384/ASPH轴是AS病变发生的一个关键机制.
通过准miR-384/ASPH通路,Circ_0005699干扰为动脉样硬化提供了潜在的治疗途径.

关键词:

在 AS AS AS 中,这是一种ASPH.圆周_000569999 年月日在HUVECs中,在 miR-384 的位置上.

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