The research group of Zhang Lili, a professor of neurology at the Field Surgery Institute of Daping Hospital, Third Military Medical University, found that PPARγ (peroxisome proliferator-activated receptor-γ) is mediated by inhibiting TLR4 (Toll-like receptor 4) in vascular smooth muscle cells Inflammatory response, improve vascular intimal hyperplasia, and provide new ideas for clinical treatment of vascular hyperplasia. Related research was published in the British authoritative journal "Cardiovascular Research" recently.
Intimal hyperplasia is not only an important pathological feature of atherosclerosis, but also the main reason for the failure of vascular reconstruction surgery. Inhibiting the migration and proliferation of vascular smooth muscle cells (VSMC) is an important strategy to prevent arterial intimal hyperplasia.
PPARγ is a nuclear receptor transcription factor that regulates diabetes, atherosclerosis and other diseases by regulating the expression of various genes involved in glucose and fat metabolism. Studies by Zhang Lili and others found that PPARγ agonist rosiglitazone can significantly reduce mouse carotid artery intimal hyperplasia caused by guide wire injury; in vitro experiments, up-regulation of PPARγ expression can inhibit the proliferation and migration of cultured VSMCs.
In order to further explore the mechanism of PPARγ inhibiting the migration and proliferation of VSMC and preventing arterial intimal hyperplasia, the research team further detected the inflammation response regulated by PPARγ and found that there is a cross-link between PPARγ and TLR4-mediated inflammation. Activating PPARγ can significantly reduce the expression of TLR4 and inflammatory factors in mouse carotid artery after guide wire injury; up-regulating PPARγ expression in vitro experiments can also inhibit the expression of TLR4 and inflammatory factors in VSMC. The activation of TLR4 can significantly reduce the inhibitory effect of PPARγ on the proliferation and migration of VSMC. Compared with normal VSMC, PPARγ had no significant effect on the proliferation and migration ability of TLR4-deficient VSMC. The above results show that the lack of TLR4 can affect the role of PPARγ in regulating VSMC proliferation and migration, suggesting that the process of PPARγ inhibition of VSMC proliferation and migration may be mediated by TLR4 signaling pathway.
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