ArticleThe Journal of clinical investigation2015
Macrophages mediate cardioprotective cellular postconditioning in acute myocardial infarction.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 1 of them a synthesis that pooled it.
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Who cites it
144 citing papers in PubMed, 1 synthesis or guideline pooled it, 238 citations in OpenAlex.
- Comparative Effectiveness of Anti-Inflammatory Drug Treatments in Coronary Heart Disease Patients: A Systematic Review and Network Meta-Analysis.Mediators of inflammation · 2021Pooled it
- Prevention of atrial fibrillation after open-chest surgery with extracellular vesicle therapy.JCI insight · 2023Trial
- Targeting NR4A1 (Nur77) in Macrophage Polarization: Molecular Mechanisms and Translational Prospects for Cardiac Repair After Myocardial Infarction.International journal of molecular sciences · 2026Review
- Cardiosphere-Derived Cells from Not Dilated and Dilated Human Myocardium Exhibit Enhanced Metabolic Potential Compared with Conventional Cardiac Mesenchymal Stem/Stromal Cells.International journal of molecular sciences · 2026Article
- From marrow memory to adverse ventricular remodeling: trained immunity after myocardial infarction.Frontiers in immunology · 2026Review
- Immunometabolic regulation of cardiac macrophages in heart failure with preserved ejection fraction.Frontiers in immunology · 2026Review
- Augmentation of DNA exonuclease TREX1 in macrophages as a therapy for cardiac ischemic injury.Science translational medicine · 2025Article
- Exosome‑mediated crosstalk between the cardiovascular and musculoskeletal systems: Mechanisms and therapeutic potential (Review).International journal of molecular medicine · 2025Review
- Quercetin improves myocardial ischemia-reperfusion injury by regulating macrophage M2 polarization through Bcl-2/Beclin-1 complex.European journal of medical research · 2025Article
- Review
- Macrophage Polarization in Myocardial Ischemia‒Reperfusion Injury: Pathophysiology and Therapeutic Targets.Drug design, development and therapy · 2025Review
- Global requirements for manufacturing and validation of clinical grade extracellular vesicles.The journal of liquid biopsy · 2024Review
- Deconstructing Regenerative Medicine: From Mechanistic Studies of Cell Therapy to Novel Bioinspired RNA Drugs.Circulation research · 2024Review
- Non-coding RNA yREX3 from human extracellular vesicles exerts macrophage-mediated cardioprotection via a novel gene-methylating mechanism.European heart journal · 2024Article
- Y4 RNA fragments from cardiosphere-derived cells ameliorate diabetic myocardial ischemia‒reperfusion injury by inhibiting protein kinase C β-mediated macrophage polarization.Cardiovascular diabetology · 2024Article
- Review
- Early Impairment of Paracrine and Phenotypic Features in Resident Cardiac Mesenchymal Stromal Cells after Thoracic Radiotherapy.International journal of molecular sciences · 2024Article
- Cardiac fibrogenesis: an immuno-metabolic perspective.Frontiers in physiology · 2024Review
- MSC-Derived Exosomes Mitigate Myocardial Ischemia/Reperfusion Injury by Reducing Neutrophil Infiltration and the Formation of Neutrophil Extracellular Traps.International journal of nanomedicine · 2024Article
- The complex landscape of DMD mutations: moving towards personalized medicine.Frontiers in genetics · 2024Review
84 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic injury in the heart induces an inflammatory cascade that both repairs damage and exacerbates scar tissue formation. Cardiosphere-derived cells (CDCs) are a stem-like population that is derived ex vivo from cardiac biopsies; they confer both cardioprotection and regeneration in acute myocardial infarction (MI). While the regenerative effects of CDCs in chronic settings have been studied extensively, little is known about how CDCs confer the cardioprotective process known as cellular postconditioning. Here, we used an in vivo rat model of ischemia/reperfusion (IR) injury-induced MI and in vitro coculture assays to investigate how CDCs protect stressed cardiomyocytes. Compared with control animals, animals that received CDCs 20 minutes after IR had reduced infarct size when measured at 48 hours. CDCs modified the myocardial leukocyte population after ischemic injury. Specifically, introduction of CDCs reduced the number of CD68+ macrophages, and these CDCs secreted factors that polarized macrophages toward a distinctive cardioprotective phenotype that was not M1 or M2. Systemic depletion of macrophages with clodronate abolished CDC-mediated cardioprotection. Using both in vitro coculture assays and a rat model of adoptive transfer after IR, we determined that CDC-conditioned macrophages attenuated cardiomyocyte apoptosis and reduced infarct size, thereby recapitulating the beneficial effects of CDC therapy. Together, our data indicate that CDCs limit acute injury by polarizing an effector macrophage population within the heart.
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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.