Apolipoprotein J Attenuates Vascular Restenosis by Promoting Autophagy and Inhibiting the Proliferation and Migration of Vascular Smooth Muscle Cells

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.

Automated summary

This research investigated the role of CLU in regulating VSMC proliferation and migration in vascular restenosis. The findings showed that CLU was highly expressed in vascular restenosis and over-expression of CLU promoted VSMC autophagy, thus attenuating intimal hyperplasia and vascular restenosis.