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盖莱克7通过抵制干扰流量诱导的内皮细胞到介质细胞过渡来减轻腹腔大动脉动脉瘤的进展

Yanbing Wang^1,2,3, Yilin Zhou^1,2,3, Yeshen Zhang⁴

¹Department of Cardiology, State Key Laboratory of Organ Failure Research, Nanfang Hospital, Southern Medical University, Guangzhou, China.

|January 29, 2026

概括

内皮转介质过渡 (EndMT) 驱动腹腔大动脉动脉瘤 (AAA). 盖莱克-7通过阻止通过CREB的SRGN转录,限制TGFβ/smad通路来抑制EndMT和AAA的进展.

科学领域:

血管生物学血管生物学
细胞生物学细胞生物学
分子医学是分子医学.

背景情况:

由流动干扰 (d-flow) 诱导的内皮细胞 (ECs) 中的内皮细胞到介质细胞过渡 (EndMT) 是炎症性血管疾病的关键因素.
腹腔大动脉动脉瘤 (AAA) 是一种具有复杂病原性的显著血管疾病.
研究EndMT及其在AAA中的潜在机制的作用对于治疗开发至关重要.

研究的目的:

阐明EndMT在腹腔大动脉动脉瘤 (AAA) 的发展中的作用.
在AAA中确定加勒-7对EndMT的调节背后的分子机制.
探索基于EndMT调制的AAA潜在的治疗点.

主要方法:

在人类和小鼠AAA模型中评估d-flow诱导的EndMT,使用免疫阻塞,免疫光和电子显微镜.
使用伊比迪系统诱导人类大动脉内皮细胞 (HAEC) 的d流,并通过腺相关病毒操纵加勒-7的表达.
采用单细胞RNA测序来探索加勒-7介导的EndMT机制并识别核心基因.

主要成果:

与抑制的加勒-7相关的d流诱导的EndMT与AAA正相关.
增强的加勒-7表达减弱了d流诱导的EndMT和AAA进展.
减少的加勒-7表达加剧了EndMT和AAA的进展,SRGN被确定为由加勒-7和CREB调节的核心基因,影响TGFβ/smad通路.

结论:

在d流下的EC中EndMT是AAA发展的关键驱动力.
富含内皮质的加勒-7作为d流诱导的EndMT和AAA进展的抑制剂.
盖莱克-7通过竞争性结合CREB来抑制SRGN转录,从而限制TGFβ/smad通路的激活,并防止AAA的进展.

关键词:

腹部大动脉动脉瘤腹部大动脉动脉瘤干扰了流动的干扰.内皮细胞是内皮细胞.内皮细胞到介质细胞的过渡.盖莱克-7-7的使用方法

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