{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T04:11:44Z","timestamp":1782360704925,"version":"3.54.5"},"reference-count":40,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2017,9,14]],"date-time":"2017-09-14T00:00:00Z","timestamp":1505347200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004192","name":"National Science and Technology Development Agency Thailand","doi-asserted-by":"crossref","award":["RSA5880015"],"award-info":[{"award-number":["RSA5880015"]}],"id":[{"id":"10.13039\/501100004192","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Chiang Mai University Center of Excellence Award"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovascular Therapeutics"],"published-print":{"date-parts":[[2017,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Aim<\/jats:title><jats:p>Although the gold standard treatment for acute myocardial infarction is reperfusion therapy, reperfusion itself can cause myocardial damage via induction of cardiac mitochondrial dysfunction. This can lead to increased myocardial infarct size, arrhythmias, and left ventricular (<jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content>) dysfunction. Recently, a newly discovered peptide, Humanin, has been shown to exert several beneficial effects including antioxidative and antiapoptosis effects. We recently reported that a Humanin analogue (<jats:styled-content style=\"fixed-case\">HNG<\/jats:styled-content>, 84\u00a0\u03bcg\/kg) given prior to cardiac ischemia exerted cardioprotection against I\/R injury, but failed to do so when it was given after ischemia was induced. However, in a clinical setting, patients can only be treated after the onset of ischemia. In this study, we investigated the potential benefit of various doses of <jats:styled-content style=\"fixed-case\">HNG<\/jats:styled-content> therapy (84, 168, 252\u00a0\u03bcg\/kg) against myocardial I\/R injury when applied during ischemia on cardiac arrhythmia, myocardial infarct size, cardiac mitochondrial function, and <jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content> function.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Myocardial I\/R injury was induced in rats by 30\u2010minute left anterior descending coronary artery occlusion, followed by 120\u2010minute of reperfusion. <jats:styled-content style=\"fixed-case\">HNG<\/jats:styled-content> at the different doses were given intravenously at 15\u00a0minutes after ischemic onset and also at the onset of reperfusion.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">HNG<\/jats:styled-content> (252\u00a0\u03bcg\/kg) applied during the ischemic period not only increased <jats:styled-content style=\"fixed-case\">HN<\/jats:styled-content> levels in the damaged myocardium, but also significantly decreased cardiac arrhythmia, myocardial infarct size, cardiac mitochondrial dysfunction, and left ventricular dysfunction. These benefits were mediated through the attenuation of cardiac mitochondrial dysfunction.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>High\u2010dose <jats:styled-content style=\"fixed-case\">HN<\/jats:styled-content> applied during ischemia in rats could exert cardioprotection against I\/R injury<jats:bold>\u2010<\/jats:bold>induced mitochondrial dysfunction.<\/jats:p><\/jats:sec>","DOI":"10.1111\/1755-5922.12289","type":"journal-article","created":{"date-parts":[[2017,7,20]],"date-time":"2017-07-20T08:18:50Z","timestamp":1500538730000},"source":"Crossref","is-referenced-by-count":39,"title":["High\u2010dose Humanin analogue applied during ischemia exerts cardioprotection against ischemia\/reperfusion injury by reducing mitochondrial dysfunction"],"prefix":"10.1111","volume":"35","author":[{"given":"Savitree","family":"Thummasorn","sequence":"first","affiliation":[{"name":"Cardiac Electrophysiology Research and Training Center Faculty of Medicine Chiang Mai University  Chiang Mai Thailand"},{"name":"Cardiac Electrophysiology Unit Department of Physiology Faculty of Medicine Chiang Mai University  Chiang Mai Thailand"},{"name":"Center of Excellence in Cardiac Electrophysiology Research Chiang Mai University  Chiang Mai Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Krekwit","family":"Shinlapawittayatorn","sequence":"additional","affiliation":[{"name":"Cardiac Electrophysiology Research and Training Center Faculty of Medicine Chiang Mai University  Chiang Mai Thailand"},{"name":"Cardiac Electrophysiology Unit Department of Physiology Faculty of Medicine Chiang Mai University  Chiang Mai Thailand"},{"name":"Center of Excellence in Cardiac Electrophysiology Research Chiang Mai University  Chiang Mai Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Siriporn C.","family":"Chattipakorn","sequence":"additional","affiliation":[{"name":"Cardiac Electrophysiology Research and Training Center 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