{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T07:29:40Z","timestamp":1792654180829,"version":"4.5.0"},"reference-count":57,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2016,8]]},"abstract":"<jats:sec>\n                    <jats:title>Objective\u2014<\/jats:title>\n                    <jats:p>Drug-eluting coronary stents reduce restenosis rate and late lumen loss compared with bare-metal stents; however, drug-eluting coronary stents may delay vascular healing and increase late stent thrombosis. The peroxisome proliferator\u2013activated receptor-delta (PPAR\u03b4) exhibits actions that could favorably influence outcomes after drug-eluting coronary stents placement.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Approach and Results\u2014<\/jats:title>\n                    <jats:p>Here, we report that PPAR\u03b4 ligand\u2013coated stents strongly reduce the development of neointima and luminal narrowing in a rabbit model of experimental atherosclerosis. Inhibition of inflammatory gene expression and vascular smooth muscle cell (VSMC) proliferation and migration, prevention of thrombocyte activation and aggregation, and proproliferative effects on endothelial cells were identified as key mechanisms for the prevention of restenosis. Using normal and PPAR\u03b4-depleted VSMCs, we show that the observed effects of PPAR\u03b4 ligand GW0742 on VSMCs and thrombocytes are PPAR\u03b4 receptor dependent. PPAR\u03b4 ligand treatment induces expression of pyruvate dehydrogenase kinase isozyme 4 and downregulates the glucose transporter 1 in VSMCs, thus impairing the ability of VSMCs to provide the increased energy demands required for growth factor\u2013stimulated proliferation and migration.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions\u2014<\/jats:title>\n                    <jats:p>In contrast to commonly used drugs for stent coating, PPAR\u03b4 ligands not only inhibit inflammatory response and proliferation of VSMCs but also prevent thrombocyte activation and support vessel re-endothelialization. Thus, pharmacological PPAR\u03b4 activation could be a promising novel strategy to improve drug-eluting coronary stents outcomes.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.115.306962","type":"journal-article","created":{"date-parts":[[2016,6,9]],"date-time":"2016-06-09T22:53:55Z","timestamp":1465512835000},"page":"1534-1548","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":27,"title":["Activation of Peroxisome Proliferator\u2013Activated Receptor-\u03b4 as Novel Therapeutic Strategy to Prevent In-Stent Restenosis and Stent Thrombosis"],"prefix":"10.1161","volume":"36","author":[{"given":"Jarkko","family":"Hyt\u00f6nen","sequence":"first","affiliation":[{"name":"From the Department of Molecular Medicine, A.I. Virtanen Institute, University of Eastern Finland, Kuopio, Finland (J.H., S.Y.-H.); Centre for R&amp;D, Uppsala University\/County Council of Gaevleborg, Gaevle, Sweden (O.L.); Institute for Pathology, University Clinic of Schleswig-Holstein, Campus Kiel, Kiel, Germany (J.H.B.); Max-Delbr\u00fcck Center for Molecular Medicine, Berlin, Germany (W.-H.S., D.M., A.H., J.-D.D., L.T., F.B.); Department of Cardiology (B.P., F.B.) and Center for Cardiovascular..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olli","family":"Lepp\u00e4nen","sequence":"additional","affiliation":[{"name":"From the Department of Molecular Medicine, A.I. 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