{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T06:00:07Z","timestamp":1788328807026,"version":"build-2803163510"},"reference-count":26,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,12,13]],"date-time":"2016-12-13T00:00:00Z","timestamp":1481587200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovascular Therapeutics"],"published-print":{"date-parts":[[2017,2]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Aims<\/jats:title><jats:p>Glycogen synthase kinase\u20103\u03b2 (<jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>\u20103\u03b2) and mitochondrial permeability transition pore (<jats:styled-content style=\"fixed-case\">mPTP<\/jats:styled-content>) play an important role in myocardial ischemia\u2013reperfusion injury. The aim of this study was to investigate whether postconditioning with rosuvastatin is able to reduce myocardial ischemia\u2013reperfusion injury and clarify the potential mechanisms.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Isolated rat hearts underwent 30\u00a0minutes of ischemia and 60\u00a0minutes of reperfusion in the presence or absence of rosuvastatin (1\u201050\u00a0nmol\/L). The activity of signaling pathway was determined by Western blot analysis, and Ca<jats:sup>2+<\/jats:sup>\u2010induced <jats:styled-content style=\"fixed-case\">mPTP<\/jats:styled-content> opening was assessed by the use of a potentiometric method.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Rosuvastatin significantly reduced myocardial infarct size and improved cardiac function at 5 and 10\u00a0nmol\/L. Protection disappeared at higher concentration and reverted to increased damage at 50\u00a0nmol\/L. At 5\u00a0nmol\/L, rosuvastatin increased the phosphorylation of protein kinase B (Akt) and <jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>\u20103\u03b2, concomitant with a higher Ca<jats:sup>2+<\/jats:sup> load required to open the <jats:styled-content style=\"fixed-case\">mPTP<\/jats:styled-content>. Rosuvastatin postconditioning also significantly increased superoxide dismutase activity and reduced malondialdehyde and radical oxygen species level. <jats:styled-content style=\"fixed-case\">LY<\/jats:styled-content>294002, phosphatidylinositol\u20103\u2010kinase (<jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>3K) inhibitors, abolished these protective effects of rosuvastatin postconditioning.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Rosuvastatin prevents myocardial ischemia\u2013reperfusion injury by inducing phosphorylation of <jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>3K\u2013Akt and <jats:styled-content style=\"fixed-case\">GSK<\/jats:styled-content>\u20103\u03b2, preventing oxidative stress and subsequent inhibition of <jats:styled-content style=\"fixed-case\">mPTP<\/jats:styled-content> opening.<\/jats:p><\/jats:sec>","DOI":"10.1111\/1755-5922.12225","type":"journal-article","created":{"date-parts":[[2016,8,31]],"date-time":"2016-08-31T18:23:09Z","timestamp":1472667789000},"page":"3-9","source":"Crossref","is-referenced-by-count":43,"title":["Rosuvastatin postconditioning protects isolated hearts against ischemia\u2013reperfusion injury: The role of radical oxygen species, <scp>PI<\/scp>3K\u2013Akt\u2013<scp>GSK<\/scp>\u20103\u03b2 pathway, and mitochondrial permeability transition pore"],"prefix":"10.1111","volume":"35","author":[{"given":"Chun\u2010Wei","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Cardiology Tianjin Medical University Tianjin Chest Hospital  Tianjin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fan","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Diagnostic Ultrasound Tianjin Medical University Cancer Institute and Hospital National Clinical Research Center of Cancer Key Laboratory of Cancer Prevention and Therapy  Tianjin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shi\u2010Zhao","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Thoracic Surgery Tianjin Chest Hospital  Tianjin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yue","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Cardiology Tianjin Medical University Tianjin Chest Hospital  Tianjin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liang\u2010Hui","family":"Wan","sequence":"additional","affiliation":[{"name":"Department of Cardiology Tianjin Medical University Tianjin Chest Hospital  Tianjin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong\u2010Liang","family":"Cong","sequence":"additional","affiliation":[{"name":"Department of Cardiology Tianjin Medical University Tianjin Chest Hospital  Tianjin 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