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We began analyzing https://www.nature.com/articles/ncomms4303, but it redirected us to https://www.nature.com/articles/ncomms4303. The analysis below is for the second page.

Title[redir]:
IRF8 suppresses pathological cardiac remodelling by inhibiting calcineurin signalling | Nature Communications
Description:
Interferon regulatory factor 8 (IRF8) is known to affect the innate immune response, for example, by regulating the differentiation and function of immune cells. However, whether IRF8 can influence cardiac hypertrophy is unknown. Here we show that IRF8 levels are decreased in human dilated/hypertrophic cardiomyopathic hearts and in murine hypertrophic hearts. Mice overexpressing Irf8 specifically in the heart are resistant to aortic banding (AB)-induced cardiac hypertrophy, whereas mice lacking IRF8 either globally or specifically in cardiomyocytes develop an aggravated phenotype induced by pressure overload. Mechanistically, we show that IRF8 directly interacts with NFATc1 to prevent NFATc1 translocation and thus inhibits the hypertrophic response. Inhibition of NFATc1 ameliorates the cardiac abnormalities in IRF8βˆ’/βˆ’ mice after AB. In contrast, constitutive activation of NFATc1 nullifies the protective effects of IRF8 on cardiac hypertrophy in IRF8-overexpressing mice. Our results indicate that IRF8 is a potential therapeutic target in pathological cardiac hypertrophy. The transcription factor interferon regulatory factor 8 (IRF8) is known to regulate differentiation and function of immune cells. Here the authors show that IRF8 is upregulated in the hypertrophic heart in humans and mice, where it suppresses cardiac remodelling by inhibiting calcineurin signalling.

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Keywords {πŸ”}

irf, cardiac, mice, hypertrophy, nfatc, fig, pubmed, article, supplementary, google, scholar, analysis, cas, hearts, results, cells, protein, experimental, group, cell, pathological, heart, staining, expression, weeks, data, hypertrophic, pressure, performed, factor, response, levels, transcription, statistical, signalling, cardiomyocytes, nfat, irftg, nature, ang, central, factors, nrcms, interferon, effects, western, nuclear, gene, activity, compared,

Topics {βœ’οΈ}

nature portfolio privacy policy advertising nature myocyte-enriched calcineurin-interacting protein egfp-myc-irf8 recombinant plasmid yield canfatc1-cre-tg mice 0/ reprints produce cardiac-specific irf8-tg linearized Ξ±-mhc-irf8 plasmid mem-cre-tg mice served replication-defective adenoviral vectors wayne bond lau c-terminal flag-tagged canfatc1 Ξ±-myosin heavy chain confocal laser-scanning microscope adnfatc1-luc/bnp-luc/mcip1 ab-operated irf8-tg mice calcineurin inhibitors cabin1/cain ab-induced cardiac hypertrophy Ξ²-myosin heavy chain human dendritic-cell immunodeficiency lv end-diastolic dimension lv end-systolic dimension generate egfp-myc-irf8Ξ΄200–377 induce cre-dependent recombination full size image irf8 deficiency aggravates diluted media cytosolic pattern-recognition receptors nox2 mediate tcf/lef l-type ca2+ channel author correspondence calcineurin-dependent transcriptional pathway calcineurin/nfat coupling participates n-terminal hemagglutinin-tagged ab-induced nuclear translocation consensus sequence-binding protein cardiac-specific canfatc1-tg m-mode images derived social media rna-protein scaffold complex glutathione-sepharose 4b beads nfat-mediated transcriptional activation24 serum-free dmem/f12 nramp1-mediated innate resistance pure c57bl/6j background real-time pcr assays xue-hai zhu psi-egfp-myc-c1

Schema {πŸ—ΊοΈ}

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      headline:IRF8 suppresses pathological cardiac remodelling by inhibiting calcineurin signalling
      description:Interferon regulatory factor 8 (IRF8) is known to affect the innate immune response, for example, by regulating the differentiation and function of immune cells. However, whether IRF8 can influence cardiac hypertrophy is unknown. Here we show that IRF8 levels are decreased in human dilated/hypertrophic cardiomyopathic hearts and in murine hypertrophic hearts. Mice overexpressing Irf8 specifically in the heart are resistant to aortic banding (AB)-induced cardiac hypertrophy, whereas mice lacking IRF8 either globally or specifically in cardiomyocytes develop an aggravated phenotype induced by pressure overload. Mechanistically, we show that IRF8 directly interacts with NFATc1 to prevent NFATc1 translocation and thus inhibits the hypertrophic response. Inhibition of NFATc1 ameliorates the cardiac abnormalities in IRF8Γ’ΒˆΒ’/Γ’ΒˆΒ’ mice after AB. In contrast, constitutive activation of NFATc1 nullifies the protective effects of IRF8 on cardiac hypertrophy in IRF8-overexpressing mice. Our results indicate that IRF8 is a potential therapeutic target in pathological cardiac hypertrophy. The transcription factor interferon regulatory factor 8 (IRF8) is known to regulate differentiation and function of immune cells. Here the authors show that IRF8 is upregulated in the hypertrophic heart in humans and mice, where it suppresses cardiac remodelling by inhibiting calcineurin signalling.
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      name:Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China
      name:Cardiovascular Research Institute of Wuhan University, Wuhan, China

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