Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction

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...

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Autores principales:	Veronika Zach, Felix Lucas Bähr, Frank Edelmann
Formato:	article
Lenguaje:	EN
Publicado:	Radcliffe Medical Media 2020
Materias:	Diseases of the circulatory (Cardiovascular) system RC666-701
Acceso en línea:	https://doaj.org/article/57e92d1e8d0b496e8595bd47bf1ccf5b
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spelling	oai:doaj.org-article:57e92d1e8d0b496e8595bd47bf1ccf5b2021-12-04T16:02:32ZSuppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction10.15420/cfr.2019.102057-75592057-7540https://doaj.org/article/57e92d1e8d0b496e8595bd47bf1ccf5b2020-03-01T00:00:00Zhttps://www.cfrjournal.com/articleindex/cfr.2019.10https://doaj.org/toc/2057-7540https://doaj.org/toc/2057-7559Heart 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.Veronika ZachFelix Lucas BährFrank EdelmannRadcliffe Medical MediaarticleDiseases of the circulatory (Cardiovascular) systemRC666-701ENCardiac Failure Review , Vol 6, Iss , Pp - (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Diseases of the circulatory (Cardiovascular) system RC666-701
spellingShingle	Diseases of the circulatory (Cardiovascular) system RC666-701 Veronika Zach Felix Lucas Bähr Frank Edelmann Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction
description	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.
format	article
author	Veronika Zach Felix Lucas Bähr Frank Edelmann
author_facet	Veronika Zach Felix Lucas Bähr Frank Edelmann
author_sort	Veronika Zach
title	Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction
title_short	Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction
title_full	Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction
title_fullStr	Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction
title_full_unstemmed	Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction
title_sort	suppression of tumourigenicity 2 in heart failure with preserved ejection fraction
publisher	Radcliffe Medical Media
publishDate	2020
url	https://doaj.org/article/57e92d1e8d0b496e8595bd47bf1ccf5b
work_keys_str_mv	AT veronikazach suppressionoftumourigenicity2inheartfailurewithpreservedejectionfraction AT felixlucasbahr suppressionoftumourigenicity2inheartfailurewithpreservedejectionfraction AT frankedelmann suppressionoftumourigenicity2inheartfailurewithpreservedejectionfraction
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Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction

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