Abstract
The interleukin-33 (IL-33)/ suppression of tumorigenicity 2 (ST2) pathway is a potential pathophysiological mediator of cardiac fibrosis. Soluble ST2 (sST2) is one of the main isoforms of ST2 with strong prognostic value in cardiac disease. The exact role of sST2 in cardiac fibrosis is unknown. The aim of this study was 1) to investigate myocardial expression of the IL-33/ST2 pathway in relation to myocardial fibrosis in end-stage heart failure patients and 2) to study whether plasma sST2 is associated with histologically determined cardiac fibrosis.
Highlights
Associate Editor Craig Stolen oversaw the review of this articleElectronic supplementary material The online version of this article contains supplementary material, which is available to authorized users.Utrecht, The Netherlands 4 Division of Heart and Lungs, Department of Cardiology, UniversityMedical Center Utrecht, Heidelberglaan 100, Room F.01.1.46, In-house postbox E.03.511, Post office box. 85500, 3508 GA Utrecht, The NetherlandsHeart failure is a progressive disease with a large burden on public health [1, 2]
All patients were in New York Heart Association (NYHA) class IV and received an left ventricular assist device (LVAD) as bridge to transplantation between January 2010 and October 2013
We found significant correlations between the myocardial Soluble Suppression of tumorigenicity 2 (ST2) (sST2) and IL-33 mRNA expression and the amount of fibrosis, suggesting a potential role of the IL-33/ST2 pathway in cardiac fibrosis
Summary
The Netherlands 4 Division of Heart and Lungs, Department of Cardiology, University. Heart failure is a progressive disease with a large burden on public health [1, 2]. This clinical syndrome is a result of initial injury or stress followed by remodeling of the myocardium leading to changes in size, shape, and function of the heart [3, 4]. In contrast to state-of-the-art imaging techniques, biomarkers are considered mechanistically driven and clinically more useful predictors of ventricular remodeling [5]
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