木素是一种内源调节器,可触发血管退化,解剖和破裂
Lihong Pan1,2,3, Peiyuan Bai4,2,3, Xinyu Weng4,2,3
1Institutes of Biomedical Sciences, Fudan University, Shanghai, China (L.P., S.C., A.S., J.G.).
通过使血管光滑肌细胞转化,促进胸腔大动脉解剖 (TAD). 在巨细胞中抑制LGMN可能为TAD预防和治疗提供一种新的治疗策略.
科学领域:
- 心血管生物学
- 分子医学
- 血管生物学
背景情况:
- 胸前动脉剖析 (TAD) 涉及细胞外矩阵降解和血管光滑肌细胞 (VSMC) 现型切换.
- 莱古马因 (LGMN) 参与细胞外基质降解,但其在VSMC分化和TAD发病过程中的作用尚不清楚.
研究的目的:
- 研究LGMN在VSMC分化中的作用及其对胸前动脉剖析 (TAD) 的贡献.
主要方法:
- 从公开的微阵列数据集中选差异表达的基因.
- 使用Lgmn淘汰小鼠 (包括巨特异性) 和BAPN诱导的TAD模型.
- 进行RNA测序,细胞共同培养试验,共免疫沉和同位分析.
主要成果:
- 在TAD患者和小鼠的大动脉和血清中,LGMN的调节升高.
- 缺少或抑制Lgmn可改善TAD的进展和细胞外基质的降解.
- 通过与整合蛋白αvβ3相互作用,抑制了巨菌衍生LGMN的VSMC分化,从而加剧了TAD.
结论:
- 尤其是巨细胞的LGMN信号传递在TAD的发展中起着至关重要的作用.
- 向LGMN为胸前大动脉解剖提供了潜在的新疗法.
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