title: IL-33 attenuates cardiac remodeling following myocardial infarction via inhibition of the p38 MAPK and NF-κB pathways.
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.
authors.affiliation: Department of Cardiology Ward 1, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
authors.forename: Honglei
authors.initials: H
authors.lastname: Yin
authors.affiliation: Department of Cardiology Ward 1, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
authors.forename: Peicheng
authors.initials: P
authors.lastname: Li
authors.affiliation: Department of Cardiology Ward 1, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
authors.forename: Fudong
authors.initials: F
authors.lastname: Hu
authors.affiliation: Department of Cardiology Ward 1, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
authors.forename: Yakun
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Cardiology Ward 1, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Chai
authors.affiliation: Department of Cardiology Ward 1, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D004195:Disease Models, Animal; D004452:Echocardiography; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D000067596:Interleukin-33; D007378:Interleukins / Q000494:pharmacology*; D051379:Mice; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism*; D010766:Phosphorylation / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects*; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling / Q000187:drug effects*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: C506535:Il33 protein, mouse; D000067596:Interleukin-33; D007378:Interleukins; D016328:NF-kappa B; D048051:p38 Mitogen-Activated Protein Kinases