ArticleThe Journal of clinical investigation2021
Basophils balance healing after myocardial infarction via IL-4/IL-13.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 84 citations in OpenAlex.
- Immuno-instructive biomaterials for coronary artery disease and myocardial infarction repair.Journal of materials science. Materials in medicine · 2026Review
- Basophils drive the resolution and promote wound healing in adult and aged mice.The Journal of experimental medicine · 2026Article
- Sensitizer-Induced Basophils Accelerate Skin Re-Epithelialization via IL-4/IL-13-Mediated Macrophage Polarization.Allergy · 2026Article
- Development of a Novel Prognostic Inflammation Index to Predict Poor Outcomes in Patients With Intracerebral Hemorrhage: A Longitudinal Study.CNS neuroscience & therapeutics · 2026Article
- Fibrosis-memory is mediated by IL-3-producing T cells and drives progression of fibrosis.The Journal of clinical investigation · 2026Article
- Immune Mechanisms in Myocardial Remodeling Following Myocardial Infarction: Focusing on Regulatory Networks of T Cell Responses.Journal of inflammation research · 2026Review
- Basophils activate splenic B cells and dendritic cells via IL-13 signaling in acute traumatic brain injury.Journal of neuroinflammation · 2025Article
- Emerging roles of basophils in the resolution of acute respiratory distress syndrome.The European respiratory journal · 2025Article
- The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Single-cell transcriptome reveals the reprogramming of immune microenvironment during the transition from MASH to HCC.Molecular cancer · 2025Article
- Temporal single-cell sequencing analysis reveals that GPNMB-expressing macrophages potentiate muscle regeneration.Experimental & molecular medicine · 2025Article
- Injection of ROS-Responsive Hydrogel Loaded with IL-1β-targeted nanobody for ameliorating myocardial infarction.Bioactive materials · 2025Article
- Basophils induce protumorigenic cytokines from A549 lung adenocarcinoma via mechanisms requiring IgE, galectin-3, and IL-3 priming.Journal of leukocyte biology · 2025Article
- Tissue macrophages: origin, heterogenity, biological functions, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- Exploring the Mechanism of Action of Berberine on Arrhythmia After Myocardial Infarction: A Network Pharmacology, Molecular Docking, and Cellular Experimental Study.Cardiovascular therapeutics · 2025Article
- Transient Inhibition of Translation Improves Cardiac Function After Ischemia/Reperfusion by Attenuating the Inflammatory Response.Circulation · 2024Article
- Basophils Play a Protective Role in the Recovery of Skin Barrier Function from Mechanical Injury in Mice.The Journal of investigative dermatology · 2024Article
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Myocardial Inflammation in Heart Failure With Reduced and Preserved Ejection Fraction.Circulation research · 2024Review
- IL-4 attenuates myocardial infarction injury by promoting M2 macrophage polarization.Annals of medicine and surgery (2012) · 2024Article
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Authors and funding
19 authors at 7 institutions in 2 countries.
Funding
Abstract
The inflammatory response after myocardial infarction (MI) is a precisely regulated process that greatly affects subsequent remodeling. Here, we show that basophil granulocytes infiltrated infarcted murine hearts, with a peak occurring between days 3 and 7. Antibody-mediated and genetic depletion of basophils deteriorated cardiac function and resulted in enhanced scar thinning after MI. Mechanistically, we found that basophil depletion was associated with a shift from reparative Ly6Clo macrophages toward increased numbers of inflammatory Ly6Chi monocytes in the infarcted myocardium. Restoration of basophils in basophil-deficient mice by adoptive transfer reversed this proinflammatory phenotype. Cellular alterations in the absence of basophils were accompanied by lower cardiac levels of IL-4 and IL-13, two major cytokines secreted by basophils. Mice with basophil-specific IL-4/IL-13 deficiency exhibited a similarly altered myeloid response with an increased fraction of Ly6Chi monocytes and aggravated cardiac function after MI. In contrast, IL-4 induction in basophils via administration of the glycoprotein IPSE/α-1 led to improved post-MI healing. These results in mice were corroborated by the finding that initially low counts of blood basophils in patients with acute MI were associated with a worse cardiac outcome after 1 year, characterized by a larger scar size. In conclusion, we show that basophils promoted tissue repair after MI by increasing cardiac IL-4 and IL-13 levels.
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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.