IL-33 attenuates cardiac remodeling following myocardial infarction via inhibition of the p38 MAPK and NF-κB pathways Retraction in /10.3892/mmr.2022.12868

Yin,Honglei; Li,Peicheng; Hu,Fudong; Wang,Yakun; Chai,Xiaoyan; Zhang,Yan

doi:10.3892/mmr.2014.2051

IL-33 attenuates cardiac remodeling following myocardial infarction via inhibition of the p38 MAPK and NF-κB pathways

Retraction in: /10.3892/mmr.2022.12868

Authors:
- Honglei Yin
- Peicheng Li
- Fudong Hu
- Yakun Wang
- Xiaoyan Chai
- Yan Zhang
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Affiliations: Department of Cardiology Ward 1, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China, Department of Cardiology Ward 1, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China
Published online on: March 14, 2014 https://doi.org/10.3892/mmr.2014.2051
Pages: 1834-1838

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Abstract

The inflammatory response has adverse effects on left ventricular (LV) function and remodeling post-myocardial infarction (MI). Interleukin (IL)-33 is considered to have anti-inflammatory properties. The present study examined whether the suppression of inflammation with IL-33 was able to attenuate LV dysfunction and remodeling post-MI. The MI model was induced and the mice were treated with either saline or recombinant IL-33. Inflammatory mediators, LV functional changes and structural remodeling were evaluated. IL-33 significantly suppressed macrophage infiltration and the production of inflammatory cytokines in the myocardium. IL-33 treatment significantly improved LV function, reduced infarct size and infarct wall thinning. MI-induced activation of the p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-κB (NF-κB) pathways was also suppressed. Our data demonstrated that IL-33 suppresses inflammatory responses and improved LV function and remodeling by inhibiting the p38 MAPK and NF-κB pathways. IL-33 may be a potential therapeutic target for heart dysfunction post-MI.

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