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However, reperfusion itself can cause myocardial damage due to increased reactive oxygen species (<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>) production, a process known as ischemia\/reperfusion (I\/R) injury. Cardiac mitochondria are the major organelle of <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> production in the heart. Cardiac mitochondrial dysfunction caused by an increased <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> production can increase cardiac arrhythmia incidence, myocardial infarct size, and cardiac dysfunction. Thus, preservation of cardiac mitochondrial function is a promising pharmacological approach to reduce cardiac I\/R injury. Humanin (HN), a newly discovered 24\u2010amino acid polypeptide, has been shown to exert antioxidative stress and antiapoptotic effects. Although the cardioprotective effects of HN against I\/R injury has been reported, the effect of HN on cardiac mitochondrial function has not yet been investigated. Thus, we tested the hypothesis that HN exerts its cardioprotective effects against I\/R injury through the attenuation of cardiac mitochondrial dysfunction.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>I\/R protocol was carried out using a 30\u2010minutes occlusion of a left anterior descending coronary artery followed by a 120\u2010minutes of reperfusion. The plasma HN level, infarct size, arrhythmia incidence, left ventricular function, and cardiac mitochondrial function were determined.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Endogenous HN level before I\/R injury showed no difference between groups, but was markedly decreased after I\/R injury. HN analogue pretreatment decreased arrhythmia incidence and infarct size, improved cardiac mitochondrial function, and attenuated cardiac dysfunction.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Humanin analogue pretreatment exerted cardioprotective effects against I\/R injury through the attenuation of cardiac mitochondrial dysfunction.<\/jats:p><\/jats:sec>","DOI":"10.1111\/1755-5922.12210","type":"journal-article","created":{"date-parts":[[2016,7,19]],"date-time":"2016-07-19T13:48:20Z","timestamp":1468936100000},"page":"404-414","source":"Crossref","is-referenced-by-count":57,"title":["Humanin exerts cardioprotection against cardiac ischemia\/reperfusion injury through attenuation of mitochondrial dysfunction"],"prefix":"10.1111","volume":"34","author":[{"given":"Savitree","family":"Thummasorn","sequence":"first","affiliation":[{"name":"Cardiac Electrophysiology Research and Training Center Faculty of Medicine Chiang Mai University  Chiang Mai 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