ArticleAging2021
Deferoxamine accelerates endothelial progenitor cell senescence and compromises angiogenesis.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 10 citations in OpenAlex.
- Iron Dysregulation and Vascular Diseases: A Contemporary Review.Journal of the American Heart Association · 2026Review
- Pathological features of the lateral joint capsule and lateral retinaculum in lateral patellar compression syndrome: a retrospective case-control study.BMC musculoskeletal disorders · 2026Article
- Apoptotic vesicles from endothelial cells promote endothelial progenitor cell differentiation and angiogenesis via miR-30a-5p mediated activation of the EGFR/PI3K/AKT/VEGF pathway.Stem cell research & therapy · 2026Article
- Elucidating the effect of deferoxamine, a hypoxia mimetic agent, on angiogenesis restoration in endothelial progenitor cells (EPCs) from diabetic mice.Iranian journal of basic medical sciences · 2025Article
- CCL4 contributes to aging related angiogenic insufficiency through activating oxidative stress and endothelial inflammation.Angiogenesis · 2024Article
- Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescence reduces the circulating number and angiogenic activity of endothelial progenitor cells (EPCs), and is associated with aging-related vascular diseases. However, it is very time-consuming to obtain aged cells (~1 month of repeated replication) or animals (~2 years) for senescence studies. Here, we established an accelerated senescence model by treating EPCs with deferoxamine (DFO), an FDA-approved iron chelator. Four days of low-dose (3 μM) DFO induced senescent phenotypes in EPCs, including a senescent pattern of protein expression, impaired mitochondrial bioenergetics, altered mitochondrial protein levels and compromised angiogenic activity. DFO-treated early EPCs from young and old donors (< 35 vs. > 70 years old) displayed similar senescent phenotypes, including elevated senescence-associated β-galactosidase activity and reduced relative telomere lengths, colony-forming units and adenosine triphosphate levels. To validate this accelerated senescence model
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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.