ArticleJournal of cellular and molecular medicine2014
Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 58 citations in OpenAlex.
- Cardiometabolic disease management: influences from epigenetics.Epigenomics · 2025Review
- 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
- 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
- Epigenetic Regulation of Endothelial Cell Function by Nucleic Acid Methylation in Cardiac Homeostasis and Disease.Cardiovascular drugs and therapy · 2021Review
- YAP/TAZ deficiency reprograms macrophage phenotype and improves infarct healing and cardiac function after myocardial infarction.PLoS biology · 2020Article
- Screening ginseng saponins in progenitor cells identifies 20(R)-ginsenoside RhScientific reports · 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
- Decitabine assists umbilical cord-derived mesenchymal stem cells in improving glucose homeostasis by modulating macrophage polarization in type 2 diabetic mice.Stem cell research & therapy · 2019Article
- Epigenetic reprogramming of immune cells in injury, repair, and resolution.The Journal of clinical investigation · 2019Review
- Epigenetic control of macrophage polarization: implications for targeting tumor-associated macrophages.Oncotarget · 2018Review
- Epigenetic Regulation of Myofibroblast Phenotypes in Fibrosis.Current pathobiology reports · 2018Article
- Functional Relevance of Macrophage-mediated Inflammation to Cardiac Regeneration.Chonnam medical journal · 2018Review
- Macrophage polarization and function: new prospects for fibrotic disease.Immunology and cell biology · 2017Review
- DNA methylation regulated gene expression in organ fibrosis.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- Azacytidine Treatment Inhibits the Progression of Herpes Stromal Keratitis by Enhancing Regulatory T Cell Function.Journal of virology · 2017Article
- The cardioprotective efficacy of TVP1022 against ischemia/reperfusion injury and cardiac remodeling in rats.Pharmacology research & perspectives · 2016Article
- Novel concepts in radiation-induced cardiovascular disease.World journal of cardiology · 2016Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We examined whether a shift in macrophage phenotype could be therapeutic for myocardial infarction (MI). The mouse macrophage cell line RAW264.7 was stimulated with peptidoglycan (PGN), with or without 5-azacytidine (5AZ) treatment. MI was induced by ligation of the left anterior descending coronary artery in rats, and the rats were divided into two groups; a saline-injection group and a 5AZ-injection group (2.5 mg/kg/day, intraperitoneal injection). LV function was evaluated and immunohistochemical analyses were performed 2 weeks after MI. Cardiac fibrosis was induced by angiotensin II (AngII) infusion with or without 5AZ (5 mg/kg/day) in mice. Nitric oxide was produced by PGN, which was reduced by 77.87% after 5AZ treatment. Both induction of inducible nitric oxide synthase (iNOS) and iNOS promoter activity by PGN were inhibited by 5AZ. Ejection fraction (59.00 ± 8.03% versus 42.52 ± 2.58%), contractility (LV dP/dt-max, 8299.76 ± 411.56 mmHg versus 6610.36 ± 282.37 mmHg) and relaxation indices (LV dP/dt-min, -4661.37 ± 210.73 mmHg versus -4219.50 ± 162.98 mmHg) were improved after 5AZ administration. Cardiac fibrosis in the MI+5AZ was 8.14 ± 1.00%, compared with 14.93 ± 2.98% in the MI group (P < 0.05). Arginase-1(+)CD68(+) macrophages with anti-inflammatory phenotype were predominant in the infarct border zone of the MI+5AZ group, in comparison with the MI group. AngII-induced cardiac fibrosis was also attenuated after 5AZ administration. In cardiac fibroblasts, pro-fibrotic mediators and cell proliferation were increased by AngII, and these increases were attenuated after 5AZ treatment. 5AZ exerts its cardiac protective role through modulation of macrophages and cardiac fibroblasts.
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