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Biomarkers of IL-33 and sST2 and Lack of Association with Carvedilol Therapy in Heart Failure

Authors Firouzabadi N, Dashti M, Dehshahri A, Bahramali E

Received 1 April 2020

Accepted for publication 29 May 2020

Published 12 June 2020 Volume 2020:12 Pages 53—58


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Professor Arthur Frankel

Negar Firouzabadi,1– 3 Maryam Dashti,1 Ali Dehshahri,4 Ehsan Bahramali5

1Department of Pharmacology and Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran; 2Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran; 3Noncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran; 4Department of Pharmaceutical Biotechnology, Shiraz University of Medical Sciences, Shiraz, Iran; 5Digestive Disease Research Center, Digestive Disease Research Institute, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran

Correspondence: Negar Firouzabadi
Department of Pharmacology and Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran
Tel +98-917-314-5303
Fax +98-713-2424128

Objective: The IL-33/ST2 pathway plays a fundamental role in the cardiovascular system and can be considered as a new therapeutic strategy for the treatment or prevention of cardiovascular diseases. ST2, as an interleukin (IL)-1 receptor family member, has transmembrane (ST2L) and soluble (sST2) isoforms. sST2 neutralizes IL-33 and thereby inhibits the cardioprotective role of IL-33/ST2L signaling pathway. Increase in sST2 level is associated with weak cardiac output and can be a predictor of mortality in heart failure (HF). Thereby, we hypothesized that there may be a relationship between the cardioprotective effects of carvedilol and sST2 and IL-3 in HF patients.
Methods: sST2 and IL-33 were measured in serum of 66 individuals; 22 healthy volunteers and 44 suffering from HF; among whom 25 patients received carvedilol and the other 19 patients did not receive any β-blockers.
Results: Lack of association between serum levels of IL-33 and sST2 was observed between HF patients and healthy individuals (2.4466 ± 0.69 vs 2.6748 ± 0.33 and 3416.6 ± 1089.1 vs 2971.6 ± 792.5, respectively). Our results indicated no significant difference between sST2 and IL-33 levels in HF patients who did not receive beta-blockers and patients receiving carvedilol (P=0.59 and P=0.97).
Conclusion: Our results showed a lack of association between serum levels of IL-33 and sST2 and HF. Moreover, the results do not confirm the cardioprotective mechanism of carvedilol by means of IL-33/sST2 pathway.

Keywords: heart failure, IL-33, sST2, carvedilol, β-blocker, biomarker

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