Key result
CTP synthase 1 (CTPS1) inhibitors and other smooth muscle-specific targets are promising agents for next-generation drug-eluting stents to prevent stent thrombosis without blocking re-endothelialization.
Targeting CTPS1 and other cell-specific factors may allow for next-generation drug-eluting stents that inhibit smooth muscle proliferation without impairing essential re-endothelialization.
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May inform targeted stent design to reduce thrombosis while preserving healing; leaves open the need for clinical validation.
The occurrence of stent thrombosis is one of the major obstacles limiting the long-term clinical efficacy of percutaneous coronary intervention. The anti-smooth muscle proliferation drugs coated on drug-eluting stents (DES) often indistinguishably block re-endothelialization, an essential step toward successful vascular repair, due to their nonspecific effect on endothelial cells (ECs). Therefore, identification of therapeutic targets that differentially regulate vascular smooth muscle cell (VSMC) and EC proliferation may lead to the development of ideal drugs for the next-generation DES. Our recent studies have shown that CTP synthase 1 (CTPS1) differentially regulates the proliferation of VSMC and EC after vascular injury. Therefore, CTPS1 inhibitors are promising agents for DES. In addition to CTPS1, other factors have also shown cell-specific effects on VSMC and/or EC proliferation and thus may become potential molecular targets for developing drugs to coat stents.
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Tang et al. (2013) conducted a review in Stent thrombosis following percutaneous coronary intervention. CTPS1 inhibitors and smooth muscle-specific drug targets was evaluated. CTP synthase 1 (CTPS1) inhibitors and other smooth muscle-specific targets are promising agents for next-generation drug-eluting stents to prevent stent thrombosis without blocking re-endothelialization.
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