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O304通过AMPK/mTOR/MMP通路激活缓解腹腔大动脉动脉瘤的形成

Daohan Sun¹, Yaming Du¹

¹Department of Vascular Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, China.

Frontiers in pharmacology

|December 16, 2024

概括

新型AMPK激动剂O304通过激活AMPK通路并抑制血管光滑肌细胞 (VSMC) 现型切换来防止腹腔大动脉动脉瘤 (AAA) 的形成. 这项研究强调O304作为AAA的潜在治疗剂.

科学领域:

心血管研究研究心血管研究
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

腹腔大动脉动脉瘤 (AAA) 破裂是老年人死亡的主要原因.
目前对AAA的药理干预措施在手术治疗之前是有限的.
氨酸单酸激活蛋白激酶 (AMPK) 信号在AAA病变发生中的作用需要进一步阐明.

研究的目的:

评估AAA形成中新型AMPK激动剂O304的调节作用.
探索O304在AAA中的作用的潜在分子机制.
调查O304对血管光滑肌细胞 (VSMC) 表型和AMPK信号传递的影响.

主要方法:

在小鼠AAA样本中通过RT-qPCR评估AMPK途径组件和VSMC相关基因.
使用了转变生长因子-β (TGF-β) 诱导的VSMC表型切换和小鼠AAA模型的体外模型.
分析了O304对VSMC表型,AMPK信号传递,AAA直径和血压的影响,使用免疫光学,西方斑点,ELISA和RT-qPCR.

主要成果:

在AAA样本中,AMPK信号传递和收缩VSMC基因的下调.
O304激活了AMPK信号,防止了VSMC从收缩型到合成型的表型在体外转换.
在体内,O304激活了AMPK,增加了收缩性VSMC,并减少了小鼠的AAA形成和血压.

结论:

从收缩到繁殖的VSMC表型切换与AAA发育期间AMPK通路的抑制有关.
作为AMPK激动剂,O304可以逆转这种开关,从而抑制AAA的形成.
使用O304等药物向AMPK通路,对AAA具有显著的治疗潜力.

关键词:

这就是AMPKK.第304章这是什么?腹部大动脉动脉瘤腹部大动脉动脉瘤收缩性血管光滑肌肉细胞细胞收缩性血管在mTOROR中使用mTOR.

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