Elevated adropin: A candidate diagnostic marker for myocardial infarction in conjunction with troponin-I

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dc.contributor.authorAydin, Suna
dc.contributor.authorKuloglu, Tuncay
dc.contributor.authorAydin, Suleyman
dc.contributor.authorKalayci, Mehmet
dc.contributor.authorYilmaz, Musa
dc.contributor.authorCakmak, Tolga
dc.contributor.authorEren, Mehmet Nesimi
dc.date.accessioned2024-04-24T16:15:49Z
dc.date.available2024-04-24T16:15:49Z
dc.date.issued2014
dc.departmentDicle Üniversitesien_US
dc.description.abstractMyocardial infarction (MI; heart attack) can cause injury to or death of heart muscle tissue (myocardium) owing to prolonged ischemia and hypoxia. Troponins and CK-MB are released from heart muscle cells during MI. It has been demonstrated that energy expenditure is regulated by adropin expressed in the endocardium, myocardium, and epicardium. We hypothesized that adropin is released into the bloodstream during myocardial muscle injury caused by MI, so the serum level rises as myocytes die. Therefore, we examined the association between adropin expression and myocardial infarction in isoproterenol-induced myocardial infarction. Rats were randomly allocated to six groups. After treatment they were decapitated and their blood and tissues were collected for adropin measurement. Changes in adropin synthesis in rat heart, kidney and liver tissues in isoproterenol (ISO)-induced MI were demonstrated immunohistochemically. Serum adropin concentrations were measured by ELISA, and troponin-I, CK and CK-MB concentrations by autoanalysis. The results demonstrated that cardiac muscle cells, glomerular, peritubular and renal cortical interstitial cells, hepatocytes and liver sinusoidal cells all synthesize adropin, and synthesis increased 1-24 h after MI except in the liver cells. The findings elucidate the pathogenesis of MI, and the gradual increase in serum adropin could be a novel diagnostic marker and serve as an alternative to troponin-I measurement for diagnosing MI. (C) 2014 Elsevier Inc. All rights reserved.en_US
dc.identifier.doi10.1016/j.peptides.2014.06.001
dc.identifier.endpage97en_US
dc.identifier.issn0196-9781
dc.identifier.issn1873-5169
dc.identifier.pmid24932661
dc.identifier.scopus2-s2.0-84905961563
dc.identifier.scopusqualityQ2
dc.identifier.startpage91en_US
dc.identifier.urihttps://doi.org/10.1016/j.peptides.2014.06.001
dc.identifier.urihttps://hdl.handle.net/11468/15933
dc.identifier.volume58en_US
dc.identifier.wosWOS:000340307800016
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherElsevier Science Incen_US
dc.relation.ispartofPeptides
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectMyocardial Infarctionen_US
dc.subjectAdropinen_US
dc.subjectCardiac Muscle Cellsen_US
dc.subjectHepatocytesen_US
dc.subjectKidneysen_US
dc.titleElevated adropin: A candidate diagnostic marker for myocardial infarction in conjunction with troponin-Ien_US
dc.titleElevated adropin: A candidate diagnostic marker for myocardial infarction in conjunction with troponin-I
dc.typeArticleen_US

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