Department of Cardiovascular, Tianjin Chest Hospital, Tianjin, 300222, China.
J Cardiovasc Transl Res. 2022 Oct;15(5):1086-1099. doi: 10.1007/s12265-022-10227-y. Epub 2022 Mar 4.
This research investigated the mechanism of CLU in vascular restenosis by regulating vascular smooth muscle cell (VSMC) proliferation and migration. Firstly, rat models of balloon injury (BI) were established, followed by the assessment of the injury to the common carotid artery. The effect of CLU on the intimal hyperplasia of BI rats was measured after the intervention in CLU, in addition to the evaluation of proliferation, migration, and autophagy of VSMCs. Moreover, the interaction between ATG and LC3 was analyzed, followed by validation of the role of autophagy in CLU's regulation on the proliferation and migration of VSMCs. It was found that CLU was highly expressed in BI rats. Altogether, our findings indicated that CLU was highly expressed in vascular restenosis, and CLU over-expression promoted the binding between ATG3 and LC3, thus facilitating VSMC autophagy and eventually attenuating intimal hyperplasia and vascular restenosis.
本研究通过调节血管平滑肌细胞（VSMC）增殖和迁移来探讨 CLU 在血管再狭窄中的作用机制。首先，建立大鼠球囊损伤（BI）模型，然后评估颈总动脉损伤。在 CLU 干预后，测量 CLU 对 BI 大鼠内膜增生的影响，同时评估 VSMC 的增殖、迁移和自噬。此外，分析 ATG 和 LC3 之间的相互作用，验证自噬在 CLU 调节 VSMC 增殖和迁移中的作用。结果发现，CLU 在 BI 大鼠中高表达。总之，我们的研究结果表明，CLU 在血管再狭窄中高表达，CLU 过表达促进 ATG3 与 LC3 的结合，从而促进 VSMC 自噬，最终减轻内膜增生和血管再狭窄。
