ArticleScientific reports2015
5-Azacytidine modulates interferon regulatory factor 1 in macrophages to exert a cardioprotective effect.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 55 citations in OpenAlex.
- Epigenetic‑ncRNA crosstalk in atherosclerosis: Mechanisms, disease progression and therapeutic potential (Review).International journal of molecular medicine · 2025Review
- PANoptosis: a potential target of atherosclerotic cardiovascular disease.Apoptosis : an international journal on programmed cell death · 2025Review
- Uncovering dendritic cell specific biomarkers for diagnosis and prognosis of cardiomyopathy using single cell RNA sequencing and comprehensive bioinformatics analysis.Scientific reports · 2025Article
- Cardiometabolic disease management: influences from epigenetics.Epigenomics · 2025Review
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- IKKε-deficient macrophages impede cardiac repair after myocardial infarction by enhancing the macrophage-myofibroblast transition.Experimental & molecular medicine · 2024Article
- A review on regulation of DNA methylation during post-myocardial infarction.Frontiers in pharmacology · 2024Review
- Epigenetics in Heart Failure: Role of DNA Methylation in Potential Pathways Leading to Heart Failure with Preserved Ejection Fraction.Biomedicines · 2023Review
- Epigenetic regulation of macrophage polarization in wound healing.Burns & trauma · 2023Review
- Construction of a Band-Aid Like Cardiac Patch for Myocardial Infarction with Controllable HAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Recent Advances in Designing Electroconductive Biomaterials for Cardiac Tissue Engineering.Advanced healthcare materials · 2022Review
- Tregs biomimetic nanoparticle to reprogram inflammatory and redox microenvironment in infarct tissue to treat myocardial ischemia reperfusion injury in mice.Journal of nanobiotechnology · 2022Article
- The Prospective Application of Melatonin in Treating Epigenetic Dysfunctional Diseases.Frontiers in pharmacology · 2022Review
- Article
- YAP/TAZ deficiency reprograms macrophage phenotype and improves infarct healing and cardiac function after myocardial infarction.PLoS biology · 2020Article
- Macrophage Activities in Myocardial Infarction and Heart Failure.Cardiology research and practice · 2020Review
- Antiinflammatory activity of ANGPTL4 facilitates macrophage polarization to induce cardiac repair.JCI insight · 2019Article
- Adjuvant role of macrophages in stem cell-induced cardiac repair in rats.Experimental & molecular medicine · 2018Article
- Epigenetic signatures in cardiac fibrosis, special emphasis on DNA methylation and histone modification.Heart failure reviews · 2018Review
- Epigenetic control of macrophage polarization: implications for targeting tumor-associated macrophages.Oncotarget · 2018Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are actively involved in inflammatory responses during the progression of cardiac injury, including myocardial infarction (MI). A previous study showed that 5-azacytidine (5AZ), a DNA methylation inhibitor, can ameliorate cardiac injury by shifting macrophages toward an anti-inflammatory phenotype via iNOS inhibition. Here, we show that the beneficial effect of 5AZ is associated with sumoylation of interferon regulatory factor-1 (IRF1) in macrophages. IRF1 is a critical transcription factor for iNOS induction and is antagonized by IRF2. In the stimulated macrophages, IRF1 accumulated in the nucleus without degradation by 5AZ treatment. In animal study, 5AZ administration resulted in significant improvements in cardiac function and fibrosis. IRF1-expressing macrophages were more abundant in the 5AZ-treated MI group than in the PBS-treated MI group. Because sumoylated IRF1 is known to mimic IRF2, we examined the IRF1 sumoylation. Sumoylated IRF1 was resistant to degradation and significantly increased in the 5AZ-treated MI group. Collectively, 5AZ had a protective effect after MI by potentiation of IRF1 sumoylation and is suggested as a novel therapeutic intervention for cardiac repair.
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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.