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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Dr. Yasunori Ueda,
View the Slides from this session in ESC Congress 365
In this session, some interesting mechanisms involved in the process of restenosis were introduced with the suggestion of potential treatment options. Prof. Marie-Luce Bochaton-Piallat (Geneva, CH) explained that extracellular S100A4 would play an important role in the smooth muscle cell phenotype change between contractile and synthetic, which might be a therapeutic target to prevent restenosis.
Prof. Lina Badimon (Barcelona, ES) explained that tissue factor would contribute to restenotic lesion formation by inducing smooth muscle cell migration through Wnt signaling.
Prof. Ciro Indorfi (Catanzaro, IT) explained that microRNAs would affect smooth muscle cell phenotype switch and endothelial cell response to injury. He showed, using in vivo balloon injury model, that the inhibition of microRNA (miR-92a) by an antagomir would increase endothelial formation and reduce neointimal hyperplasia.
Prof. Frank van Buuren (Bad Oeynhausen, DE) explained that stent surface modification by anti-CD34 antibody would enhance stent endothelization. He emphasized that enhancing endothelization by stent surface modification would be important to prevent restenosis, because conventional drugs used in drug-eluting stent are potent cytotoxic with adverse effect on endothelization.
The 2nd generation drug-eluting stents has already achieved relatively good outcome with low incidence of thrombosis and restenosis; however, they still have a problem of very late stent failure. Furthermore, as the merit of absorbable stent (scaffold) that allows the recovery of vessel motion and remodeling has been recognized, we may need new technologies to reduce the restenosis in the absorbable scaffold that might be mainly due to smooth muscle cell proliferation. Some of the new treatment strategies discussed in this session may help developing better drug-eluting stents or absorbable scaffolds in the near future.
Cellular and molecular mechanisms in vascular restenosis
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