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在调节血管内皮细胞功能障碍和衰老中的miR-34a-5p/MARCHF8/ADAM10轴

Zonghao Qian¹, Yuzhen Huang¹, Ni Yang¹

¹Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China; Key Laboratory of Vascular Aging, Ministry of Education, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, China.

Mechanisms of ageing and development

|April 13, 2025

概括

血管衰老涉及内皮细胞衰老. 一项新的研究确定了miR-34a-5p/MARCHF8/ADAM10通路,表明MARCHF8可以防止内皮衰老和动脉样硬化.

科学领域:

血管生物学血管生物学
细胞衰老细胞衰老
老龄化的分子机制.

背景情况:

血管衰老,以内皮功能障碍和衰老为特征,驱动心血管和代谢疾病.
在衰老的内皮细胞中ADAM10水平升高会加剧功能障碍,但其调节仍然不清楚.

研究的目的:

在衰老的内皮细胞中阐明ADAM10的调节机制.
为了研究E3泛素酶MARCHF8在内皮衰老和血管衰老中的作用.

主要方法:

在人类静脉内皮细胞 (HUVECs) 中对ADAM10进行转录后修饰分析.
MARCHF8在HUVEC中进行了敲击和过度表达的研究.
RNA测序以确定受影响的途径.
在体内研究使用高脂肪饮食养的apoE-/-小鼠.

主要成果:

在衰老的HUVEC细胞中,MARCHF8的表达减少,其降低会诱导衰老并损害内皮功能.
过度表达MARCHF8可以改善老化相关的功能障碍,并减少小鼠动脉样硬化.
miR-34a-5p的上调抑制了MARCHF8,促进了内皮老化.

结论:

一个新的miR-34a-5p/MARCHF8/ADAM10轴调节了血管内皮衰老.
MARCHF8作为对内皮衰老和动脉样硬化的保护因素.
MARCHF8是一种潜在的生物标志物和血管衰老的治疗点.

关键词:

动脉样硬化动脉样硬化细胞功能障碍和衰老的发生.人的带静脉内皮细胞在 miR-34a-5p/MARCHF8/ADAM10 调节轴上血管衰老血管衰老

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