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Review
. 2020 Mar 16:6:1-7.
doi: 10.15420/cfr.2019.10. eCollection 2020 Mar.

Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction

Affiliations
Review

Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction

Veronika Zach et al. Card Fail Rev. .

Abstract

Heart failure (HF), with steadily increasing incidence rates and mortality in an ageing population, represents a major challenge. Evidence suggests that more than half of all patients with a diagnosis of HF suffer from HF with preserved ejection fraction (HFpEF). Emerging novel biomarkers to improve and potentially guide the treatment of HFpEF are the subject of discussion. One of these biomarkers is suppression of tumourigenicity 2 (ST2), a member of the interleukin (IL)-1 receptor family, binding to IL-33. Its two main isoforms - soluble ST2 (sST2) and transmembrane ST2 (ST2L) - show opposite effects in cardiovascular diseases. While the ST2L/IL-33 interaction is considered as being cardioprotective, sST2 antagonises this beneficial effect by competing for binding to IL-33. Recent studies show that elevated levels of sST2 are associated with increased mortality in HF with reduced ejection fraction. Nevertheless, the significance of sST2 in HFpEF remains uncertain. This article aims to give an overview of the current evidence on sST2 in HFpEF with an emphasis on prognostic value, clinical association and interaction with HF treatment. The authors conclude that sST2 is a promising biomarker in HFpEF. However, further research is needed to fully understand underlying mechanisms and ultimately assess its full value.

Keywords: Heart failure; biomarker; heart failure with preserved ejection fraction; suppression of tumourigenicity 2.

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Conflict of interest statement

Disclosure: The authors have no conflicts of interest to declare.

Figures

Figure 1:
Figure 1:. Schematic Illustration of ST2/IL-33 Interaction
Figure 2:
Figure 2:. The Role of Comorbidities and Inflammatory Agents Including sST2 in the Pathophysiology of HFpEF

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