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3月2日通过调节PKM2聚合来缓解大动脉动脉瘤/剖析

Yiran E Li^1,2,3,4,5, Shuolin Liu^1,2,6,3,4,5, Litao Wang^1,2,3,4,5

¹Department of Cardiology, Shanghai Institute of Cardiovascular Diseases (Y.E.L., S.L., Litao Wang, Y.D., L. Wu, H.C., T.Z., J.L., S.X., L.L., J.G., J.R., Y.Z.), Zhongshan Hospital, Fudan University, China.

Circulation research

|March 13, 2025

概括

3月2号通过防止血管光滑肌细胞亡,作为对大动脉动脉瘤和解剖 (AAD) 的保护因素. 针对March2可能为治疗AAD提供新的治疗策略.

科学领域:

心血管生物学心血管生物学
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

大动脉动脉瘤/解剖 (AAD) 是一种严重的心血管疾病,药物治疗有限.
蛋白质ubiquitination与心血管疾病有关,但在AAD中E3 ubiquitin ligaseMarch2的作用尚不清楚.

研究的目的:

调查March2在AAD.病变发生过程中的作用.
探索March2调节血管光滑肌肉细胞亡的机制及其作为治疗点的潜力.

主要方法:

在人类AAD组织上集成的单细胞RNA测序.
生成特定于光滑肌细胞的March2淘汰赛小鼠模型.
使用β-aminopropionitrile monofumarate诱导AAD并评估March2的作用.
使用CUT&Tag-qPCR.分析基因组H3K18乳化点.

主要成果:

在人类和小鼠AAD模型中,March2表达减少.
3月2日缺陷加剧了AAD,而其恢复则拯救了病理.
3月2日与PKM2相互作用,影响K33结合的多基化,并减轻ADD诱导的基H3K18乳化.
激活PKM2可以缓解March2缺陷引起的AD严重性.

结论:

3月2日通过抑制血管光滑肌肉细胞亡,作为对AAD的内源性保护因素起作用.
3月2日成为治疗大动脉动脉瘤和剖析的有前途的治疗点.

关键词:

这是一种aminopropionitrile.一个大动脉动脉瘤.大动脉切割剖析.心血管疾病心血管疾病在任何地方都是无处不在的.

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