Department of General Surgery, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan, China.
J Cardiovasc Pharmacol. 2023 Dec 1;82(6):458-469. doi: 10.1097/FJC.0000000000001484.
Damage to the abdominal aortic wall and the local inflammatory response are key factors resulting in abdominal aortic aneurysm (AAA) formation. During this process, macrophage polarization plays a key role. However, in AAA, the regulatory mechanism of macrophages is still unclear, and further research is needed. In this study, we found that the transcription factor TCF3 was expressed at low levels in AAA. We overexpressed TCF3 and found that TCF3 could inhibit MMP and inflammatory factor expression and promote M2 macrophage polarization, thereby inhibiting the progression of AAA. Knocking down TCF3 could promote M1 polarization and MMP and inflammatory factor expression. In addition, we found that TCF3 increased miR-143-5p expression through transcriptional activation of miR-143-5p , which further inhibited expression of the downstream chemokine CCL20 and promoted M2 macrophage polarization. Our research indicates that TCF3-mediated macrophage polarization plays a key regulatory role in AAA, complementing the role and mechanism of macrophages in the occurrence and development of AAA and providing a scientific basis for AAA treatment.
腹主动脉壁损伤和局部炎症反应是导致腹主动脉瘤（AAA）形成的关键因素。在这个过程中，巨噬细胞极化起着关键作用。然而，在 AAA 中，巨噬细胞的调控机制尚不清楚，需要进一步研究。在本研究中，我们发现转录因子 TCF3 在 AAA 中表达水平较低。我们过表达 TCF3 发现 TCF3 可以抑制 MMP 和炎症因子的表达，并促进 M2 巨噬细胞极化，从而抑制 AAA 的进展。敲低 TCF3 可以促进 M1 极化和 MMP 及炎症因子的表达。此外，我们发现 TCF3 通过转录激活 miR-143-5p 增加 miR-143-5p 的表达，进一步抑制下游趋化因子 CCL20 的表达并促进 M2 巨噬细胞极化。我们的研究表明，TCF3 介导的巨噬细胞极化在 AAA 中起着关键的调节作用，补充了巨噬细胞在 AAA 的发生和发展中的作用和机制，为 AAA 的治疗提供了科学依据。
