Interleukin-33, matrix metalloproteinase-9, and tissue inhibitor of matrix metalloproteinase-1 in myocardial infarction

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dc.authorscopusid23968920100
dc.authorscopusid6506182946
dc.authorscopusid42661653300
dc.authorscopusid55635008600
dc.authorscopusid55634874600
dc.authorscopusid6507815831
dc.contributor.authorGüzel, Savaş
dc.contributor.authorSerin, Ozden
dc.contributor.authorGüzel, Eda Çelik
dc.contributor.authorBüyük, Banu
dc.contributor.authorYılmaz, Guzin
dc.contributor.authorGuvenen, Güvenç
dc.date.accessioned2022-05-11T14:12:33Z
dc.date.available2022-05-11T14:12:33Z
dc.date.issued2013
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Tıbbi Biyokimya Ana Bilim Dalı
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Aile Hekimliği Ana Bilim Dalı
dc.description.abstractBackground/Aims: Acute coronary syndrome (ACS) is characterized by increased inflammatory processes and endothelial activation. We investigated the association between ACS and inflammatory mediators and matrix-degrading enzymes. Methods: We prospectively enrolled 55 consecutive patients with ACS: 25 with unstable angina (UA) and 30 with non-ST elevated myocardial infarction (NSTEMI). For comparison, 25 age- and sex-matched subjects with no significant coronary artery stenosis were included as the control group. Peripheral serum levels of interleukin (IL)-33, matrix metalloproteinase (MMP)-9, tissue inhibitor of MMP-1, and C-reactive protein (CRP) were measured on admission, and at 12, 24, 48, and 72 hours after the initial evaluation. Results: Compared to serum levels in the control group, serum levels of IL-33 decreased in the NSTEMI group (p < 0.05), and levels of MMP-9 and tissue inhibitor of matrix metalloproteinase (TIMP)-1 increased in the UA group (p < 0.01, p < 0.05, respectively) and NSTEMI group (p < 0.05, p < 0.05, respectively). IL-33 levels were significantly lower on admission than at 12 hours after the initial evaluation (p < 0.05). IL-33 levels were negatively correlated with MMP-9 levels (r = -0.461, p < 0.05) and CRP levels (r = p < 0.05). Conclusions: Elevated levels of MMP-9, TIMP-1, and decreased levels of IL-33 play a role in the development and progression of ACS.
dc.identifier.doi10.3904/kjim.2013.28.2.165
dc.identifier.endpage173
dc.identifier.issn1226-3303
dc.identifier.issue2en_US
dc.identifier.pmid23525523
dc.identifier.scopus2-s2.0-84875492228
dc.identifier.scopusqualityQ2
dc.identifier.startpage165
dc.identifier.urihttps://doi.org/10.3904/kjim.2013.28.2.165
dc.identifier.urihttps://hdl.handle.net/20.500.11776/5599
dc.identifier.volume28
dc.identifier.wosWOS:000315703300007
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorGüzel, Savaş
dc.institutionauthorGüzel, Eda Çelik
dc.language.isoen
dc.publisherKorean Assoc Internal Medicine
dc.relation.ispartofKorean Journal of Internal Medicine
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectCoronary-Artery-Disease
dc.subjectInflammatory Cytokines
dc.subjectT-Lymphocytes
dc.subjectAtherosclerosis
dc.subjectMacrophages
dc.subjectIl-33
dc.subjectSt2
dc.subjectExpression
dc.subjectRupture
dc.subjectPlaque
dc.titleInterleukin-33, matrix metalloproteinase-9, and tissue inhibitor of matrix metalloproteinase-1 in myocardial infarction
dc.typeArticle

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