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

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) iso...

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Autores principales: Firouzabadi, Negar, Dashti, Maryam, Dehshahri, Ali, Bahramali, Ehsan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305854/
https://www.ncbi.nlm.nih.gov/pubmed/32607003
http://dx.doi.org/10.2147/CPAA.S256290
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author Firouzabadi, Negar
Dashti, Maryam
Dehshahri, Ali
Bahramali, Ehsan
author_facet Firouzabadi, Negar
Dashti, Maryam
Dehshahri, Ali
Bahramali, Ehsan
author_sort Firouzabadi, Negar
collection PubMed
description 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.
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spelling pubmed-73058542020-06-29 Biomarkers of IL-33 and sST2 and Lack of Association with Carvedilol Therapy in Heart Failure Firouzabadi, Negar Dashti, Maryam Dehshahri, Ali Bahramali, Ehsan Clin Pharmacol Original Research 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. Dove 2020-06-12 /pmc/articles/PMC7305854/ /pubmed/32607003 http://dx.doi.org/10.2147/CPAA.S256290 Text en © 2020 Firouzabadi et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Firouzabadi, Negar
Dashti, Maryam
Dehshahri, Ali
Bahramali, Ehsan
Biomarkers of IL-33 and sST2 and Lack of Association with Carvedilol Therapy in Heart Failure
title Biomarkers of IL-33 and sST2 and Lack of Association with Carvedilol Therapy in Heart Failure
title_full Biomarkers of IL-33 and sST2 and Lack of Association with Carvedilol Therapy in Heart Failure
title_fullStr Biomarkers of IL-33 and sST2 and Lack of Association with Carvedilol Therapy in Heart Failure
title_full_unstemmed Biomarkers of IL-33 and sST2 and Lack of Association with Carvedilol Therapy in Heart Failure
title_short Biomarkers of IL-33 and sST2 and Lack of Association with Carvedilol Therapy in Heart Failure
title_sort biomarkers of il-33 and sst2 and lack of association with carvedilol therapy in heart failure
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305854/
https://www.ncbi.nlm.nih.gov/pubmed/32607003
http://dx.doi.org/10.2147/CPAA.S256290
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