ArticleNature communications2014
IRF8 suppresses pathological cardiac remodelling by inhibiting calcineurin signalling.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 142 citations in OpenAlex.
- Global Evaluation of Congenital Heart Disease-Associated Non-Coding Variants.Research square · 2026Article
- Interferon regulatory factors: the next prospective targets for tissue ischemia-reperfusion injury?Frontiers in immunology · 2026Review
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- Interferon regulatory factor 5: a potential target for therapeutic intervention in inflammatory diseases.Frontiers in immunology · 2025Review
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- The Role of Interferon Regulatory Factors in Liver Diseases.International journal of molecular sciences · 2024Review
- Murine IRF8 Mutation Offers New Insight into Osteoclast and Root Resorption.Journal of dental research · 2024Article
- Endothelial cells adopt a pro-reparative immune responsive signature during cardiac injury.Life science alliance · 2024Article
- Shikonin alleviates doxorubicin-induced cardiotoxicity via Mst1/Nrf2 pathway in mice.Scientific reports · 2024Article
- Cellular zinc metabolism and zinc signaling: from biological functions to diseases and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Interferons and interferon-related pathways in heart disease.Frontiers in cardiovascular medicine · 2024Review
- The interaction between ferroptosis and inflammatory signaling pathways.Cell death & disease · 2023Review
- Article
- Review
- Isoliquiritigenin attenuates pathological cardiac hypertrophy via regulating AMPKα in vivo and in vitro.Journal of molecular histology · 2022Article
- ANGPTL8 is a negative regulator in pathological cardiac hypertrophy.Cell death & disease · 2022Article
- Lack of food intake during shift work alters the heart transcriptome and leads to cardiac tissue fibrosis and inflammation in rats.BMC biology · 2022Article
- Predicting the targets of IRF8 and NFATc1 during osteoclast differentiation using the machine learning method framework cTAP.BMC genomics · 2022Article
- RIP3 Contributes to Cardiac Hypertrophy by Influencing MLKL-Mediated Calcium Influx.Oxidative medicine and cellular longevity · 2022Article
- Liquiritin Attenuates Pathological Cardiac Hypertrophy by Activating the PKA/LKB1/AMPK Pathway.Frontiers in pharmacology · 2022Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 IRF8(-/-) 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.