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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Cardiovasc+Transl+Res
2018 ; 11
(1
): 15-21
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The Interleukin-33/ST2 Pathway Is Expressed in the Failing Human Heart and
Associated with Pro-fibrotic Remodeling of the Myocardium
#MMPMID29285671
Tseng CCS
; Huibers MMH
; van Kuik J
; de Weger RA
; Vink A
; de Jonge N
J Cardiovasc Transl Res
2018[Feb]; 11
(1
): 15-21
PMID29285671
show ga
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. In 38
patients undergoing left ventricular assist device implantation, mRNA expression
of sST2, total ST2, and IL-33 was measured in cardiac tissue obtained during the
implantation. In the same tissue, histological fibrosis was digitally quantified
and mRNA expression of pro-fibrotic signaling molecules, connective tissue growth
factor (CTGF) and transforming growth factor beta 1 (TGF?1), was measured. In
addition, plasma levels of sST2 were determined. Expression levels of IL-33/ST2
pathway factors in myocardial tissue were significantly associated with cardiac
fibrosis and the expression levels of CTGF and TGF?1. Plasma levels of sST2 did
not correlate with tissue expression of ST2, the amount of fibrosis or myocardial
expression of pro-fibrotic signaling proteins. The interleukin-33/ST2 pathway is
expressed in the failing human heart and its expression is associated with
cardiac fibrosis and pro-fibrotic signaling proteins, suggesting a role in
pro-fibrotic myocardial remodeling. Soluble ST2 levels in the circulation did not
correlate with the amount of cardiac fibrosis or myocardial ST2 expression,
however. Therefore, other pathophysiological processes such as inflammation might
also substantially affect sST2 plasma levels.