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dc.contributor.authorMcDonald, Hayley
dc.contributor.authorPeart, Jason
dc.contributor.authorKurniawan, Nyoman
dc.contributor.authorGalloway, Graham
dc.contributor.authorRoyce, Simon
dc.contributor.authorSamuel, Chrishan S
dc.contributor.authorChen, Chen
dc.date.accessioned2019-07-04T12:32:04Z
dc.date.available2019-07-04T12:32:04Z
dc.date.issued2018
dc.identifier.issn2051-817X
dc.identifier.doi10.14814/phy2.13699
dc.identifier.urihttp://hdl.handle.net/10072/381229
dc.description.abstractIschemic heart disease (IHD) is a leading cause of morbidity and mortality worldwide. Growth hormone secretagogues (GHS) have been shown to improve cardiac function in models of IHD. This study determined whether hexarelin (HEX), a synthetic GHS, preserves cardiac function and morphology in a mouse model of myocardial infarction (MI). MI was induced by ligation of the left descending coronary artery in C57BL/6J mice followed by vehicle (VEH; n = 10) or HEX (0.3 mg/kg/day; n = 11) administration for 21 days. MI‐injured and sham mice (treated with VEH; n = 6 or HEX; n = 5) underwent magnetic resonance imaging for measurement of left ventricular (LV) function, mass and infarct size at 24 h and 14 days post‐MI. MI‐HEX mice displayed a significant improvement (P < 0.05) in LV function compared with MI‐VEH mice after 14 days treatment. A significant decrease in LV mass, interstitial collagen and collagen concentration was demonstrated with chronic HEX treatment (for 21 days), accompanied by a decrease in TGF‐β1 expression, myofibroblast differentiation and an increase in collagen‐degrading MMP‐13 expression levels. Furthermore, heart rate variability analysis demonstrated that HEX treatment shifted the balance of autonomic nervous activity toward a parasympathetic predominance and sympathetic downregulation. This was combined with a HEX‐dependent decrease in troponin‐I, IL‐1β and TNF‐α levels suggestive of amelioration of cardiomyocyte injury. These results demonstrate that GHS may preserve ventricular function, reduce inflammation and favorably remodel the process of fibrotic healing in a mouse model of MI and hold the potential for translational application to patients suffering from MI.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherJohn Wiley and Sons
dc.publisher.placeUnited Kingdom
dc.relation.ispartofpagefrom1
dc.relation.ispartofpageto14
dc.relation.ispartofissue9
dc.relation.ispartofjournalPhysiological Reports
dc.relation.ispartofvolume6
dc.subject.fieldofresearchZoology
dc.subject.fieldofresearchZoology not elsewhere classified
dc.subject.fieldofresearchClinical sciences
dc.subject.fieldofresearchMedical physiology
dc.subject.fieldofresearchcode3109
dc.subject.fieldofresearchcode310999
dc.subject.fieldofresearchcode3202
dc.subject.fieldofresearchcode3208
dc.titleHexarelin treatment preserves myocardial function and reduces cardiac fibrosis in a mouse model of acute myocardial infarction
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
dcterms.licensehttp://creativecommons.org/licenses/by/4.0/
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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gro.griffith.authorPeart, Jason N.


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