ArticleJournal of the American College of Cardiology2018
Deficiency of GATA3-Positive Macrophages Improves Cardiac Function Following Myocardial Infarction or Pressure Overload Hypertrophy.
Article in Journal of the American College of Cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 77 citations in OpenAlex.
- SIK2 antagonizes postinfarction cardiac repair by driving macrophage proinflammatory and impairing efferocytosis.Science advances · 2026Article
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- Divergent roles of macrophage subsets, FoxP3, and IL-17A in HSV-1-induced CNS pathology.PLoS pathogens · 2025Article
- Engineered Endosymbionts that Modulate Primary Macrophage Function and Attenuate Tumor Growth by Shifting the Tumor Microenvironment.ACS applied bio materials · 2025Article
- Cardiac Fibrosis in the Multi-Omics Era: Implications for Heart Failure.Circulation research · 2025Review
- Identification of biomarkers associated with energy metabolism in hypertrophic cardiomyopathy and exploration of potential mechanisms of roles.Frontiers in cardiovascular medicine · 2025Article
- FABP7 in Hepatic Macrophages Promotes Fibroblast Activation and CD4Journal of immunology research · 2025Article
- Review
- Macrophage heterogeneity in myocardial infarction: Evolution and implications for diverse therapeutic approaches.iScience · 2024Review
- The association between systemic immune-inflammation index and cardiotoxicity related to 5-Fluorouracil in colorectal cancer.BMC cancer · 2024Article
- Modulation of anti-cardiac fibrosis immune responses by changing M2 macrophages into M1 macrophages.Molecular medicine (Cambridge, Mass.) · 2024Article
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Deleterious Anti-Inflammatory Macrophage Recruitment in Early Post-Infarction Phase: Unraveling the IL-6/MCP-1/STAT3 Axis.JACC. Basic to translational science · 2024Article
- Disruption of BCAA degradation is a critical characteristic of diabetic cardiomyopathy revealed by integrated transcriptome and metabolome analysis.Open life sciences · 2024Article
- An exploratory human study investigating the influence of type 2 diabetes on macrophage phenotype after myocardial infarction.International journal of cardiology. Heart & vasculature · 2023Article
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- Macrophages in cardiac remodelling after myocardial infarction.Nature reviews. Cardiology · 2023Review
- The Protective Role of TREM2 in the Heterogenous Population of Macrophages during Post-Myocardial Infarction Inflammation.International journal of molecular sciences · 2023Review
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10 authors at 1 institution in 1 country.
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Abstract
backgroundMacrophages are highly plastic cells that play an important role in the pathogenesis of cardiovascular disease.
objectivesThis study investigated the role of GATA3-positive macrophages in modulating cardiac function after myocardial infarction (MI) or in response to pressure overload hypertrophy.
methodsMyeloid-specific GATA3-deficient (mGATA3KO) mice were generated, MI or pressure overload was induced, and cardiac function was determined by echocardiography. GATA3-sufficient Cre mice were used as a control. Immunohistochemical staining, flow cytometry, MILLIPLEX Mouse Cytokine/Chemokine Assay, cultured macrophages, quantitative real-time polymerase chain reaction, and western blot were used to determine the role of GATA3 in macrophages.
resultsGATA3-positive macrophages rapidly accumulated in the infarcted region of the myocardium after acute MI. Deficiency of GATA3-positive macrophages led to a significant improvement of cardiac function in response to acute MI or pressure overload hypertrophy compared with the control mice. This improvement was associated with the presence of a large number of proinflammatory Ly6C
conclusionsWe demonstrated that the presence of GATA3-positive macrophages adversely affects remodeling of the myocardium in response to ischemia or pressure overload, whereas the absence of these macrophages led to a significant improvement in cardiac function. Targeting of signaling pathways that lead to the expression of GATA3 in macrophages may have favorable cardiac outcomes.
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