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

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Abstract

Background/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 = -0.441, 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. © 2013 The Korean Association of Internal Medicine.

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Guzel, S., Serin, O., Guzel, E. C., Buyuk, B., Yilmaz, G., & Güvenen, G. (2013). Interleukin-33, matrix metalloproteinase-9, and tissue ınhibitor of matrix metalloproteinase-1 in myocardial infarction. Korean Journal of Internal Medicine, 28(2), 165–173. https://doi.org/10.3904/kjim.2013.28.2.165

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