ArticleScience immunology2020
The myeloid type I interferon response to myocardial infarction begins in bone marrow and is regulated by Nrf2-activated macrophages.
Article in Science immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 101 citations in OpenAlex.
- Disease-associated myeloid states in cardiac remodeling: A new era of cardiac inflammation research enabled by computational biology.The journal of physiological sciences : JPS · 2026Review
- Type I IFN signaling shapes subset-specific monocyte fates in the injured myocardium.The Journal of clinical investigation · 2026Article
- Fate-mapping infiltrating monocytes following experimental myocardial infarction reveals differentiation trajectories in the infarcted heart.The Journal of clinical investigation · 2026Article
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.Advanced healthcare materials · 2026Article
- SiglecF-expressing neutrophils differentiate from mature neutrophils locally in the heart after myocardial infarction.Experimental hematology · 2026Article
- M2 macrophage exosomes reverse heart failure post-myocardial infarction by suppressing type 1 interferon signaling in myeloid cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- DNA-damaging chemotherapy reshapes cardiac-resident macrophage composition and function.Science immunology · 2026Article
- Cardiac resident macrophages: the emerging role in arrhythmogenesis.Frontiers in immunology · 2026Review
- Neutrophil Heterogeneity after Myocardial Infarction.Journal of innate immunity · 2026Review
- From marrow memory to adverse ventricular remodeling: trained immunity after myocardial infarction.Frontiers in immunology · 2026Review
- Piezo1 Upregulation in Monocyte-Derived Macrophages Impairs Post-Myocardial Infarction Cardiac Repair via Defective Efferocytosis and Enhanced Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.bioRxiv : the preprint server for biology · 2025Article
- Comparative analysis of isoproterenol- and lipopolysaccharide-mediated cytoprotective responses in the heart.American journal of physiology. Heart and circulatory physiology · 2025Article
- Mesenchymal stromal cells modulate neutrophil phenotype via paracrine signals.Stem cell research & therapy · 2025Article
- Article
- Resistin-like molecule γ attacks cardiomyocyte membranes and promotes ventricular tachycardia.Science (New York, N.Y.) · 2025Article
- Target neutrophil heterogeneity and plasticity in cancer.Journal of hematology & oncology · 2025Review
- The cGAS-STING pathway promotes acute ischemia-induced neutropoiesis and neutrophil priming in the bone marrow.Basic research in cardiology · 2025Article
- Molecular screening in a translational large animal trial identifies a differential inflammatory response for MINOCA.Basic research in cardiology · 2025Article
- CD301b+ monocyte-derived dendritic cells mediate resistance to radiotherapy.The Journal of experimental medicine · 2025Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Sterile tissue injury is thought to locally activate innate immune responses via damage-associated molecular patterns (DAMPs). Whether innate immune pathways are remotely activated remains relatively unexplored. Here, by analyzing ~145,000 single-cell transcriptomes at steady state and after myocardial infarction (MI) in mice and humans, we show that the type I interferon (IFN) response, characterized by expression of IFN-stimulated genes (ISGs), begins far from the site of injury, in neutrophil and monocyte progenitors within the bone marrow. In the peripheral blood of patients, we observed defined subsets of ISG-expressing neutrophils and monocytes. In the bone marrow and blood of mice, ISG expression was detected in neutrophils and monocytes and their progenitors, intensified with maturation at steady-state and after MI, and was controlled by Tet2 and Irf3 transcriptional regulators. Within the infarcted heart, ISG-expressing cells were negatively regulated by Nrf2 activation in Ccr2
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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.