ArticlePloS one2016
Cardiosphere-Derived Cells Facilitate Heart Repair by Modulating M1/M2 Macrophage Polarization and Neutrophil Recruitment.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Immunometabolic regulation of cardiac macrophages in heart failure with preserved ejection fraction.Frontiers in immunology · 2026Review
- Review
- Regulatory T cells: a promising new therapeutic target in ventricular remodeling after myocardial infarction.Frontiers in immunology · 2025Review
- Paintable Decellularized-ECM Hydrogel for Preventing Cardiac Tissue Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- In Search of the Holy Grail: Stem Cell Therapy as a Novel Treatment of Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2023Review
- MSC therapy ameliorates experimental gouty arthritis hinting an early COX-2 induction.Frontiers in immunology · 2023Article
- Mesh-like electrospun membrane loaded with atorvastatin facilitates cutaneous wound healing by promoting the paracrine function of mesenchymal stem cells.Stem cell research & therapy · 2022Article
- The role of major immune cells in myocardial infarction.Frontiers in immunology · 2022Review
- Effects of IL-38 on Macrophages and Myocardial Ischemic Injury.Frontiers in immunology · 2022Review
- Migration and phenotype switching of macrophages at early-phase of bone-formation by secretomes from bone marrow derived mesenchymal stem cells using rat calvaria bone defect model.Journal of dental sciences · 2022Article
- New Insights and Novel Therapeutic Potentials for Macrophages in Myocardial Infarction.Inflammation · 2021Review
- Article
- Syzygium Polyanthum Reduced TNF-α and ADAM17 Protein Expression in Myocardial Infarction Rat Model.Medical archives (Sarajevo, Bosnia and Herzegovina) · 2020Article
- CDC-derived extracellular vesicles reprogram inflammatory macrophages to an arginase 1-dependent proangiogenic phenotype.American journal of physiology. Heart and circulatory physiology · 2020Article
- Pharmacological Modulation of Cardiac Remodeling after Myocardial Infarction.Oxidative medicine and cellular longevity · 2020Review
- Article
- The effect of Substance P/Heparin conjugated PLCL polymer coating of bioinert ePTFE vascular grafts on the recruitment of both ECs and SMCs for accelerated regeneration.Scientific reports · 2019Article
- Role of Macrophages in Cardioprotection.International journal of molecular sciences · 2019Review
- Potential Role of the Resident Mesenchymal Stem-Like Cells in Renal Fibrogenesis after Ureteral Obstruction.Stem cells international · 2019Article
- Prostaglandin EJournal of the American Heart Association · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiosphere-derived cells (CDCs), one of the promising stem cell sources for myocardial repair, have been tested in clinical trials and resulted in beneficial effects; however, the relevant mechanisms are not fully understood. In this study, we examined the hypothesis that CDCs favor heart repair by switching the macrophages from a pro-inflammatory phenotype (M1) into a regulatory anti-inflammatory phenotype (M2). Macrophages from mice were cultured with CDCs-conditioned medium or with fibroblasts-conditioned medium as a control. Immunostaining showed that CDCs-conditioned medium significantly enhanced the expression of CD206 (a marker for M2 macrophages), but decreased the expression of CD86 (a marker for M1 macrophages) 3 days after culture. For animal studies, we used an acute myocardial infarction model of mice. We injected CDCs, fibroblasts, or saline only into the border zone of infarction. Then we collected the heart tissues for histological analysis 5 and 14 days after treatment. Compared with control animals, CDCs treatment significantly decreased M1 macrophages and neutrophils but increased M2 macrophages in the infarcted heart. Furthermore, CDCs-treated mice had reduced infarct size and fewer apoptotic cells compared to the controls. Our data suggest that CDCs facilitate heart repair by modulating M1/M2 macrophage polarization and neutrophil recruitment, which may provide a new insight into the mechanisms of stem cell-based myocardial repair.
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Registered trials
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.