ArticleThe Korean journal of internal medicine2013
Interleukin-33, matrix metalloproteinase-9, and tissue inhibitor [corrected] of matrix metalloproteinase-1 in myocardial infarction.
Article in The Korean journal of internal medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Galectin-3: Heart failure biomarker in pediatric heart defects.Cardiology journal · 2025Review
- Identification of biomarker panels as predictors of severity in coronary artery disease.Journal of cellular and molecular medicine · 2021Article
- Serum MMP-9 Diagnostics, Prognostics, and Activation in Acute Coronary Syndrome and Its Recurrence.Journal of cardiovascular translational research · 2018Article
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- Article
- Serum IL-33 Is a Novel Diagnostic and Prognostic Biomarker in Acute Ischemic Stroke.Aging and disease · 2016Article
- Markers of increased atherosclerotic risk in patients with chronic kidney disease: a preliminary study.Lipids in health and disease · 2016Article
- Comparison of whole blood RNA preservation tubes and novel generation RNA extraction kits for analysis of mRNA and MiRNA profiles.PloS one · 2014Article
- A novel cardiac bio-marker: ST2: a review.Molecules (Basel, Switzerland) · 2013Review
- Novel inflammatory biomarkers in acute coronary syndrome.The Korean journal of internal medicine · 2013Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsAcute 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.
methodsWe 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.
resultsCompared 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).
conclusionsElevated levels of MMP-9, TIMP-1, and decreased levels of IL-33 play a role in the development and progression of ACS.
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