ArticleAmerican journal of physiology. Heart and circulatory physiology2020
CDC-derived extracellular vesicles reprogram inflammatory macrophages to an arginase 1-dependent proangiogenic phenotype.
Article in American journal of physiology. Heart and circulatory physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 42 citations in OpenAlex.
- Small Extracellular Vesicles in Cardioprotection, Cardiac Repair, and Regeneration: Cargo Mechanisms, Producer Cell Sources, and Translational Development.Biomedicines · 2026Review
- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- Systemic and proximal tubule specific knockout ofPhysiological genomics · 2026Article
- Mechanisms and emerging research trends of angiogenesis promotion by small extracellular vesicles from different cellular sources in alleviating myocardial infarction injury.Frontiers in pharmacology · 2026Review
- Extracellular vesicles for macrophage reprogramming: an emerging paradigm in immunomodulatory therapeutics.Journal of biological engineering · 2025Review
- Augmentation of DNA exonuclease TREX1 in macrophages as a therapy for cardiac ischemic injury.Science translational medicine · 2025Article
- Extracellular vesicles in metabolic perspective: mechanism and targeted therapy.Journal of nanobiotechnology · 2025Review
- Systemic administration of allogeneic mesenchymal stem cells attenuates post-resuscitation left ventricular dysfunction in a porcine model of cardiac arrest.Resuscitation · 2025Article
- Inflammatory Cell-Targeted Delivery Systems for Myocardial Infarction Treatment.Bioengineering (Basel, Switzerland) · 2025Review
- Surface engineering enhances the therapeutic potential of systemically delivered extracellular vesicles following acute myocardial infarction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Review
- Roles of extracellular vesicles on macrophages in inflammatory bone diseases.Molecular and cellular biochemistry · 2024Review
- Extracellular vesicles containing MFGE8 from colorectal cancer facilitate macrophage efferocytosis.Cell communication and signaling : CCS · 2024Article
- Stem Cell-Derived Extracellular Vesicles in the Treatment of Cardiovascular Diseases.Pharmaceutics · 2024Review
- The Role of Extracellular Vesicles in Efferocytosis.Mini reviews in medicinal chemistry · 2024Review
- Cardiac cells and mesenchymal stem cells derived extracellular vesicles: a potential therapeutic strategy for myocardial infarction.Frontiers in cardiovascular medicine · 2024Review
- Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction.Cellular & molecular biology letters · 2023Review
- The phagocytic role of macrophage following myocardial infarction.Heart failure reviews · 2023Review
- Exosomal Non-Coding RNA Mediates Macrophage Polarization: Roles in Cardiovascular Diseases.Biology · 2023Review
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Macrophages play a pivotal role in tissue repair following myocardial infarction (MI). In response to injury, they exist along a spectrum of activation states tightly regulated by their microenvironment. Cardiosphere-derived cells (CDCs) have been shown to mediate cardioprotection via modulation of the macrophage response. Our study was designed to gain mechanistic insight into the role of CDC-derived extracellular vesicles (EVs) in modulating macrophage phenotypes and operant signaling pathways to better understand their potential contribution to immunomodulatory cardioprotection. We found that CDC-derived EVs alter the functional phenotype of macrophages, modifying levels of phagocytosis and efferocytosis without changing viability or proliferation. Interestingly, extracellular vesicles differentially regulate several M1/M2 genes dependent on macrophage activation before EV treatment but consistently upregulate arginase 1 regardless of macrophage origin or polarization state. CDC-derived EVs polarize M1 macrophages to a proangiogenic phenotype dependent on arginase 1 upregulation and independent of VEGF-A. In addition, EV-dependent arginase 1 upregulation downregulates nitric oxide (NO) secretion in activated macrophages. These data suggest a novel urea-cycle-dependent mechanism in macrophages that promotes angiogenesis and provides additional mechanistic insight into the potential contribution of CDC-derived extracellular vesicles in immunomodulatory cardioprotection.
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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.