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SGK1-介导的血管光滑肌细胞表型转变促进胸前大动脉解剖进展

Shuai Leng^1,2, Haijie Li¹, Pengfei Zhang¹

¹Department of Cardiac Surgery (S.L., H.L., P.Z., Z.D., B.S., S.X., Y.N., X.T., L.Z., H.W., N.L., F.Z., W.Y.), Central Hospital Affiliated to Shandong First Medical University, Jinan, China.

Arteriosclerosis, thrombosis, and vascular biology

|December 5, 2024

概括

血清和葡萄糖皮质激素调节激酶1 (SGK1) 通过促进血管光滑肌细胞 (VSMC) 转化来驱动胸前大动脉剖析 (TAD). 抑制SGK1或准SGK1-SIRT6-MMP9轴为TAD提供了一个潜在的治疗策略.

科学领域:

血管生物学血管生物学
分子医学是分子医学.
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

胸前大动脉剖析 (TAD) 与血管光滑肌细胞 (VSMC) 表型变化有关.
血清和葡萄糖皮质体调节激酶1 (SGK1) 在VSMC转化和TAD中的特定作用尚不清楚.

研究的目的:

研究SGK1在VSMC表型转变和TAD病原发生中的作用.
阐明将SGK1与TAD联系起来的分子机制,重点关注SGK1-SIRT6-MMP9轴.

主要方法:

使用了一种由β-aminopropionitrile monofumarate诱导的TAD小鼠模型.
使用了SGK1淘汰和药理抑制.
使用共免疫沉和质谱测量评估了蛋白质与蛋白质的相互作用.
基因表达和表观遗传修饰通过RNA测序和ChIP测试进行了分析.

主要成果:

SGK1淘汰或抑制降低了TAD发生率,并防止了细胞外基质 (ECM) 降解.
SGK1通过在Ser338的酸化促进SIRT6的降解,从而降低SIRT6蛋白水平.
SIRT6在表观遗传上抑制MMP9的表达,建立了参与ECM信号的SGK1-SIRT6-MMP9调节轴.

结论:

SGK1通过调节VSMC表型,在TAD发育中发挥关键作用.
准SGK1-SIRT6-MMP9通路为TAD提供了一种新的治疗方法.
这些发现表明TAD治疗的潜在表观遗传策略.

关键词:

剖析,胸前大动脉的切割.质谱测量质谱测量质谱测量质量测量质谱测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量质量测量序列分析,RNA序列分析,RNA序列分析这里是Sirtuinsins的所在地.无处不在的化

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