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Title:
IL-17A promotes ventricular remodeling after myocardial infarction | Journal of Molecular Medicine
Description:
Abstract Inflammatory responses play an important role in the pathogenesis of adverse ventricular remodeling after myocardial infarction (MI). We previously demonstrated that interleukin (IL)-17A plays a pathogenic role in myocardial ischemia/reperfusion injury and viral myocarditis. However, the role of IL-17A in post-MI remodeling and the related mechanisms have not been fully elucidated. Acute MI was induced by permanent ligation of the left anterior descending coronary artery in C57BL/6 mice. Repletion of IL-17A significantly aggravated both early- and late-phase ventricular remodeling, as demonstrated by increased infarct size, deteriorated cardiac function, increased myocardial fibrosis, and cardiomyocyte apoptosis. By contrast, genetic IL-17A deficiency had the opposite effect. Additional studies in vitro indicated that IL-17A induces neonatal cardiomyocyte (from C57BL/6 mice) apoptosis through the activation of p38, p53 phosphorylation, and Bax redistribution. These data demonstrate that IL-17A induces cardiomyocyte apoptosis through the p38 mitogen-activated protein kinase (MAPK)-p53-Bax signaling pathway and promotes both early- and late-phase post-MI ventricular remodeling. IL-17A might be an important target in preventing heart failure after MI. Key message • We demonstrated that IL-17A plays a pathogenic role both in the early and late stages of post-MI remodeling. • IL-17A induces murine cardiomyocyte apoptosis. • IL-17A induces murine cardiomyocyte apoptosis through the p38 MAPK-p53-Bax signaling pathway.
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article, pubmed, google, scholar, cas, myocardial, ila, apoptosis, remodeling, central, infarction, liao, ventricular, cheng, cardiomyocyte, heart, wang, zhang, interleukin, immunol, cell, research, zhou, tang, jiao, shi, role, mice, induces, access, cells, res, china, wuhan, privacy, cookies, content, journal, promotes, yuan, acute, activation, inflammation, data, information, publish, search, molecular, sufeng, jing,
Topics {✒️}
extracellular-signal-regulated protein kinases yu-hua liao & xiang cheng il-23/il-17a axis month download article/chapter il-17a significantly aggravated il-17a levels increase late-phase ventricular remodeling nf-κb-dependent suppression p38 mapk-p53 signaling wide-spread myocardial remodeling genetic il-17a deficiency celecoxib-blocked prostaglandin e2 p53-bax signaling pathway interleukin-17a induces cathepsin attenuates ventricular remodeling il-17 induces apoptosis human anti-inflammatory macrophages regulating cardiomyocyte apoptosis myocardial ischemia/reperfusion injury related subjects apolipoprotein e-deficient mice atherosclerosis-based vascular disease vascular endothelial cells yu-hua liao phosphatase-mediated crosstalk bcl-2 protein family full article pdf left ventricular remodeling preventing heart failure heart failure progression adverse ventricular remodeling il-17a plays mapk signaling pathways post-mi remodeling postmyocardial infarction remodeling adverse myocardial remodeling acute myocardial infarction interleukin-17a contributes cardiomyocyte apoptosis resveratrol-induced activation deteriorated cardiac function privacy choices/manage cookies il-17 receptor family il-17 stimulates differentiation human genome research meng-yang liao il-17-deficient mice molecular medicine aims xiang cheng p38 kinase
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headline:IL-17A promotes ventricular remodeling after myocardial infarction
description:Inflammatory responses play an important role in the pathogenesis of adverse ventricular remodeling after myocardial infarction (MI). We previously demonstrated that interleukin (IL)-17A plays a pathogenic role in myocardial ischemia/reperfusion injury and viral myocarditis. However, the role of IL-17A in post-MI remodeling and the related mechanisms have not been fully elucidated. Acute MI was induced by permanent ligation of the left anterior descending coronary artery in C57BL/6 mice. Repletion of IL-17A significantly aggravated both early- and late-phase ventricular remodeling, as demonstrated by increased infarct size, deteriorated cardiac function, increased myocardial fibrosis, and cardiomyocyte apoptosis. By contrast, genetic IL-17A deficiency had the opposite effect. Additional studies in vitro indicated that IL-17A induces neonatal cardiomyocyte (from C57BL/6 mice) apoptosis through the activation of p38, p53 phosphorylation, and Bax redistribution. These data demonstrate that IL-17A induces cardiomyocyte apoptosis through the p38 mitogen-activated protein kinase (MAPK)-p53-Bax signaling pathway and promotes both early- and late-phase post-MI ventricular remodeling. IL-17A might be an important target in preventing heart failure after MI. • We demonstrated that IL-17A plays a pathogenic role both in the early and late stages of post-MI remodeling. • IL-17A induces murine cardiomyocyte apoptosis. • IL-17A induces murine cardiomyocyte apoptosis through the p38 MAPK-p53-Bax signaling pathway.
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IL-17A
Myocardial infarction
Ventricular remodeling
Heart failure
Apoptosis
Molecular Medicine
Human Genetics
Internal Medicine
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headline:IL-17A promotes ventricular remodeling after myocardial infarction
description:Inflammatory responses play an important role in the pathogenesis of adverse ventricular remodeling after myocardial infarction (MI). We previously demonstrated that interleukin (IL)-17A plays a pathogenic role in myocardial ischemia/reperfusion injury and viral myocarditis. However, the role of IL-17A in post-MI remodeling and the related mechanisms have not been fully elucidated. Acute MI was induced by permanent ligation of the left anterior descending coronary artery in C57BL/6 mice. Repletion of IL-17A significantly aggravated both early- and late-phase ventricular remodeling, as demonstrated by increased infarct size, deteriorated cardiac function, increased myocardial fibrosis, and cardiomyocyte apoptosis. By contrast, genetic IL-17A deficiency had the opposite effect. Additional studies in vitro indicated that IL-17A induces neonatal cardiomyocyte (from C57BL/6 mice) apoptosis through the activation of p38, p53 phosphorylation, and Bax redistribution. These data demonstrate that IL-17A induces cardiomyocyte apoptosis through the p38 mitogen-activated protein kinase (MAPK)-p53-Bax signaling pathway and promotes both early- and late-phase post-MI ventricular remodeling. IL-17A might be an important target in preventing heart failure after MI. • We demonstrated that IL-17A plays a pathogenic role both in the early and late stages of post-MI remodeling. • IL-17A induces murine cardiomyocyte apoptosis. • IL-17A induces murine cardiomyocyte apoptosis through the p38 MAPK-p53-Bax signaling pathway.
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IL-17A
Myocardial infarction
Ventricular remodeling
Heart failure
Apoptosis
Molecular Medicine
Human Genetics
Internal Medicine
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