Increased levels of interleukin-6 and matrix metalloproteinase-9 are of cardiac origin in acute coronary syndrome

Shu, Jun; Ren, Ning; Du, Jibing; Zhang, Mei; Cong, Hongliang; Tigang, Huang

doi:10.1080/14017430601164263

Cited by 35 publications

(33 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…According to the available literatures, this phenomenon cannot be explained successfully. Other than the role as an inflammatory mediator in the myocardial ischemia-reperfusion process [24,25], we speculate that IL-6 may also be an inflammatory marker [26]. That is, appearance of IL-6 in the serum may reflect existence and severity of the inflammatory state.…”

Section: Discussionmentioning

confidence: 98%

Postconditioning with α7nAChR Agonist Attenuates Systemic Inflammatory Response to Myocardial Ischemia–Reperfusion Injury in Rats

et al. 2012

View full text Add to dashboard Cite

The inflammatory response plays a major role in ischemia-reperfusion injury (IRI). Considering that cholinergic stimulation can inhibit inflammatory response through the cholinergic anti-inflammatory pathway (CAP) and the α subunit-containing nicotinic acetylcholine receptor(α7nAChR) expressed by immune cells is an important component of CAP, we assessed the effect of postconditioning with α7nAChR agonist on systemic inflammatory response during the myocardial ischemia-reperfusion process in an in vivo rat model. Thirty Sprague Dawley rats were randomly divided into three groups: sham group, control group, and postconditioning with α7nAChR agonist group (PP group). In the groups other than the sham group, the left anterior descending coronary artery was ligated for 30 min followed by a 180-min reperfusion. At the end of the experiment, the serum levels of troponin I, tumor necrosis factor α, interleukin-6, and high-mobility group box 1 were assayed, and the infarct size was assessed. The results showed that postconditioning with α7nAChR agonist significantly attenuated the systemic inflammatory response to myocardial IRI, as evidenced by decreased serum levels of tumor necrosis factor α and high-mobility group box 1. Also, this treatment protected against myocardial IRI, as shown by reduced infarct size and serum troponin I level.

show abstract

Section: Discussionmentioning

confidence: 98%

Postconditioning with α7nAChR Agonist Attenuates Systemic Inflammatory Response to Myocardial Ischemia–Reperfusion Injury in Rats

et al. 2012

View full text Add to dashboard Cite

show abstract

“…124 As IL-6 is the primary cytokine of the inflammatory process 126 and inflammatory plaque destabilisation is key to plaque rupture, it has been suggested that IL-6 measurement may be useful in patients with ACS. IL-6 has been shown to be of cardiac origin in ACS 127 and to relate to other risk factors. 128 Studies have shown that IL-6 measurement is prognostic in patients with ACS, 129-131 but data are not consistent.…”

Section: Interleukinmentioning

confidence: 99%

Randomised Assessment of Treatment using Panel Assay of Cardiac markers – Contemporary Biomarker Evaluation (RATPAC CBE)

Collinson

Gaze²,

Thokala³

et al. 2013

Health Technol Assess

View full text Add to dashboard Cite

Reports are published in Health Technology Assessment (HTA) if (1) they have resulted from work for the HTA programme, and (2) they are of a sufficiently high scientific quality as assessed by the reviewers and editors.Reviews in Health Technology Assessment are termed 'systematic' when the account of the search appraisal and synthesis methods (to minimise biases and random errors) would, in theory, permit the replication of the review by others. HTA programmeThe HTA programme, part of the National Institute for Health Research (NIHR), was set up in 1993. It produces high-quality research information on the effectiveness, costs and broader impact of health technologies for those who use, manage and provide care in the NHS. 'Health technologies' are broadly defined as all interventions used to promote health, prevent and treat disease, and improve rehabilitation and long-term care.The journal is indexed in NHS Evidence via its abstracts included in MEDLINE and its Technology Assessment Reports inform National Institute for Health and Care Excellence (NICE) guidance. HTA research is also an important source of evidence for National Screening Committee (NSC) policy decisions.For more information about the HTA programme please visit the website: http://www.hta.ac.uk/ This reportThe research reported in this issue of the journal was funded by the HTA programme as project number 09/22/16. The contractual start date was in August 2010. The draft report began editorial review in February 2012 and was accepted for publication in June 2012. The authors have been wholly responsible for all data collection, analysis and interpretation, and for writing up their work. The HTA editors and publisher have tried to ensure the accuracy of the authors' report and would like to thank the reviewers for their constructive comments on the draft document. However, they do not accept liability for damages or losses arising from material published in this report.This report presents independent research funded by the National Institute for Health Research (NIHR). The views and opinions expressed by authors in this publication are those of the authors and do not necessarily reflect those of the NHS, the NIHR, NETSCC, the HTA programme or the Department of Health. Published by the NIHR Journals Library, produced by Prepress Projects Ltd, Perth, Scotland (www.prepress-projects.co.uk). Objectives: To test the diagnostic accuracy for detecting an acute myocardial infarction (AMI) using highly sensitive troponin assays and a range of new cardiac biomarkers of plaque destabilisation, myocardial ischaemia and necrosis; to test the prognostic accuracy for detecting adverse cardiac events using highly sensitive troponin assays and this range of new cardiac biomarkers; and to estimate the cost-effectiveness of using highly sensitive troponin assays or this range of new cardiac biomarkers instead of an admission and 10-to 12-hour troponin measurement. NIHR Journals LibraryDesign: Substudy of the point-of-care arm of the RATPAC (Randomised Assessment ...

show abstract

“…The myocardium is critical for the production of several inflammatory cytokines during reperfusion injury as a mechanism to start tissue repair, but it also becomes a target of their cytotoxic effects (26). For example, in patients with myocardial infarction IL-6 appears to be synthesized in the myocardium during the ischemic period and its secretion is further triggered by the reperfusion process (27, 28). Increased IL-6 is associated with poor prognosis in patients with myocardial infarction or heart failure (29) and with life-threatening events, such as shock, decreased myocardial contractility and arrhythmias (30, 31).…”

Section: Discussionmentioning

confidence: 99%

Conditional Deletion of Cardiomyocyte Peroxisome Proliferator-Activated Receptor γ Enhances Myocardial Ischemia-Reperfusion Injury in Mice

Hobson

Hake²,

O’Connor³

et al. 2014

Shock

View full text Add to dashboard Cite

The nuclear transcription factor peroxisome proliferator-activated receptor-γ (PPARγ) is a key regulator of the inflammatory response to an array of biologic insults. We have previously demonstrated that PPARγ ligands reduce myocardial ischemia-reperfusion injury in rodents. In the current study, we directly determined the role of cardiomyocyte PPARγ in ischemia-reperfusion injury, employing a model of conditional cardiomyocyte-specific deletion of PPARγ in vivo. In mice, α-myosin heavy chain-restricted Cre-mediated PPARγ deficiency was induced by tamoxifen treatment (30 mg/kg intraperitoneally) for 4 days (PPARγ−/− mice); whereas controls included mice treated with the oil diluent vehicle (PPARγ+/+ mice). Western blot and histochemical analyses confirmed that expression of PPARγ protein was abolished in cardiomyocytes of mice treated with tamoxifen, but not with vehicle. After tamoxifen or vehicle treatment, animals were subjected to 30 min ligation of the left anterior descending coronary artery followed by 2 hrs reperfusion. In PPARγ−/− mice, myocardial ischemia and reperfusion induced extensive myocardial damage, which was associated with elevated tissue activity of myeloperoxidase, indicating infiltration of neutrophils, and elevated plasma levels of troponin-I when compared to PPARγ+/+ mice. PPARγ−/− mice also demonstrated ventricular dilatation and systolic dysfunction upon echocardiographic analysis. Plasma levels of the pro-inflammatory cytokines interleukin-1β and interleukin-6 were higher in PPARγ−/− mice when compared to PPARγ+/+ mice. These pathological events in PPARγ−/− mice were associated with enhanced nuclear factor-κB DNA binding in the infarcted hearts. Thus, our data suggests that cardiomyocyte PPARγ is a crucial protective receptor and may prevent reperfusion injury by modulating mechanisms of inflammation.

show abstract

Increased levels of interleukin-6 and matrix metalloproteinase-9 are of cardiac origin in acute coronary syndrome

Abstract: Elevated levels of IL-6, hs-CRP and MMP-9 provide a link between inflammation, matrix degradation and the development and progression of ACS. IL-6 and MMP-9 appear to be released mainly from vulnerable plaque or necrotic myocardium during the acute phase of MI.

Cited by 35 publications

References 21 publications

Postconditioning with α7nAChR Agonist Attenuates Systemic Inflammatory Response to Myocardial Ischemia–Reperfusion Injury in Rats

Postconditioning with α7nAChR Agonist Attenuates Systemic Inflammatory Response to Myocardial Ischemia–Reperfusion Injury in Rats

Randomised Assessment of Treatment using Panel Assay of Cardiac markers – Contemporary Biomarker Evaluation (RATPAC CBE)

Conditional Deletion of Cardiomyocyte Peroxisome Proliferator-Activated Receptor γ Enhances Myocardial Ischemia-Reperfusion Injury in Mice

Contact Info

Product

Resources

About