ArticleJournal of nanobiotechnology2024
Macrophage-derived extracellular vesicles represent a promising endogenous iron-chelating therapy for iron overload and cardiac injury in myocardial infarction.
Article in Journal of nanobiotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed.
- Ferroptosis-driven immune remodeling in heart failure: the central role of macrophage reprogramming and impaired efferocytosis.Journal of nanobiotechnology · 2026Review
- Mapping the miRNA landscape of primitive macrophage extracellular vesicles highlights their pro-vasculogenic effects in engineered human cardiac tissue.APL bioengineering · 2026Article
- Review
- Review
- Beyond Extracellular Vesicle (EV) Hype: Practical Solutions and Remaining Hurdles in EV Research, Manufacturing, and Clinical Translation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Extracellular Vesicles in Myocardial Infarction: Dual Role in Ferroptosis Regulation and In Vivo Imaging.Diagnostics (Basel, Switzerland) · 2026Review
- Ferroptosis of smooth muscle cells in vascular diseases: from basic principles to clinical translation.Cell death discovery · 2026Review
- An Exploratory Study of Kinase Activation Profiles in Hypoxic Human Cardiomyocytes Treated with Protective Extracellular Vesicles.Research square · 2026Article
- Mechanism of Ferroptosis in Cardiovascular Disease and Its Regulation by Natural Compounds: A Narrative Review.Drug design, development and therapy · 2026Review
- Targeting Macrophage-Mediated Mechanisms in Sepsis-Induced Cardiomyopathy: From Pathophysiology to Therapeutic Strategies.Journal of inflammation research · 2026Review
- Bibliometric and visual analysis of ferroptosis in cardiovascular diseases.Journal of cardiothoracic surgery · 2025Review
- Extracellular vesicles in metabolic perspective: mechanism and targeted therapy.Journal of nanobiotechnology · 2025Review
- Iron homeostasis and ferroptosis in muscle diseases and disorders: mechanisms and therapeutic prospects.Bone research · 2025Review
- Immune in myocardial ischemia/reperfusion injury: potential mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Ferroptosis and protein translation: emerging perspectives in the research of myocardial infraction.Frontiers in cardiovascular medicine · 2025Review
- Macrophage-driven exosomes regulate the progression of cardiovascular disease.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
backgroundCardiac iron overload and ferroptosis greatly contribute to the poor prognosis of myocardial infarction (MI). Iron chelator is one of the most promising strategies for scavenging excessive iron and alleviating cardiac dysfunction post MI. However, various side effects of existing chemical iron chelators restrict their clinical application, which calls for a more viable and safer approach to protect against iron injury in ischemic hearts.
resultsIn this study, we isolated macrophage-derived extracellular vesicles (EVs) and identified macrophage-derived EVs as a novel endogenous biological chelator for iron. The administration of macrophage-derived EVs effectively reduced iron overload in hypoxia-treated cardiomyocytes and hearts post MI. Moreover, the oxidative stress and ferroptosis induced by excessive iron were considerably suppressed by application of macrophage-derived EVs. Mechanistically, transferrin receptor (TfR), which was inherited from macrophage to the surface of EVs, endowed EVs with the ability to bind to transferrin and remove excess protein-bound iron. EVs with TfR deficiency exhibited a loss of function in preventing MI-induced iron overload and protecting the heart from MI injury. Furthermore, the iron-chelating EVs were ultimately captured and processed by macrophages in the liver.
conclusionsThese results highlight the potential of macrophage-derived EVs as a powerful endogenous candidate for iron chelation therapy, offering a novel and promising therapeutic approach to protect against iron overload-induced injury in MI and other cardiovascular diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.