时空ATF3表达方式确定腹腔大动脉动脉瘤中VSMC命运
Ying Wen1, Yingying Liu1, Qiang Li2
1Institute of Pediatrics (Y.W., Y. Liu, J.T., X.F., D.L., X.F., C.C., Y.Z., W.H.T.), Guangzhou Women and Children's Medical Centre, Guangzhou Medical University, China.
Circulation research
|April 30, 2024
概括
激活转录因子3 (ATF3) 缺陷通过影响血管光滑肌细胞增殖和亡,促进腹腔大动脉动脉瘤 (AAA) 的发展. ATF3可以作为AAA的新治疗和预后标志物.
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:
- 腹腔大动脉瘤 (AAA) 是一种严重的疾病,由于对其发展的了解不足,治疗选择有限.
- 激活转录因子3 (ATF3) 被认为是心血管疾病的调节者,但其在AAA中的具体作用尚不清楚.
研究的目的:
- 研究ATF3在腹腔大动脉动脉瘤 (AAA) 的发展和进展中的作用.
- 确定ATF3作为AAA的潜在治疗和预后标志物.
主要方法:
- 在 angiotensin II (Ang II) 诱导的AAA小鼠模型中,全基因组RNA测序确定了ATF3.3.
- 在Ang II诱导的AAA小鼠中使用了血管光滑肌细胞特异的ATF3淘汰或过度表达模型.
- 在人体和小鼠血管光滑肌细胞的体外功能增益和丧失实验中,评估了ATF3对增殖和亡的影响.
主要成果:
- 在小鼠和患者的AAA组织中,ATF3的表达减少.
- 血管光滑肌细胞中的ATF3缺乏促进了AAA的形成.
- ATF3通过PDGFRB调节血管光滑肌肉细胞增殖,并通过BCL2.2抑制细胞亡.
- NFκB1和P300/BAF/H3K27ac复合体调节ATF3的转录.
结论:
- 在AAA的发展和进步中,ATF3起着至关重要的,以前未被认可的作用.
- ATF3通过调节血管光滑肌肉细胞增殖和亡来影响AAA.
- ATF3代表了潜在的新型治疗和预后标志物,用于腹腔大动脉动脉瘤.
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