Key result
IL-33 promotes vascular restenosis via intimal hyperplasia and inflammation, an effect mitigated by anti-IL-33.
Why the study?
IL-33 is associated with vascular restenosis after carotid artery balloon injury, but its involvement and mechanisms remain to be investigated.
IL-33 promotes vascular restenosis and intimal hyperplasia after carotid artery balloon injury, suggesting it may be a therapeutic target.
IL-33 may promote restenosis after vascular injury; hypothesis-generating for targeted therapies in patients.
Interleukin (IL)-33 is associated with vascular restenosis after carotid artery balloon injury. This work aims to investigate the involvement of IL-33 in carotid artery balloon injury. We first constructed carotid artery balloon injury model in male Wistar rats. Then, we found that IL-33 was highly expressed in the rats with carotid artery balloon injury 3, 14 and 21 days after surgery. Furthermore, IL-33 treatment promoted inflammatory response and carotid artery intimal hyperplasia in the rats with carotid artery balloon injury, which was effectively improved by anti-IL-33 treatment. In addition, IL-33 treatment enhanced proliferation, migration, inflammatory response and tube formation of human umbilical vein endothelial cells in a concentration-dependent way. In summary, our study demonstrates that IL-33 treatment promotes the progression of vascular restenosis after carotid artery balloon injury by enhancing carotid artery intimal hyperplasia and inflammatory response. Thus, our findings suggest that IL-33 maybe a valuable target for carotid artery balloon injury therapies.
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Zeng et al. (2020) studied Vascular restenosis after carotid artery balloon injury. IL-33 treatment vs. Anti-IL-33 treatment / Control was evaluated on Carotid artery intimal hyperplasia and inflammatory response. IL-33 treatment promoted the progression of vascular restenosis after carotid artery balloon injury by enhancing intimal hyperplasia and inflammatory response, which was improved by anti-IL-33.
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