ArticleBlood2014
Glycol-split nonanticoagulant heparins are inhibitors of hepcidin expression in vitro and in vivo.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Pooled it
- Effect of the antihepcidin Spiegelmer lexaptepid on inflammation-induced decrease in serum iron in humans.Blood · 2014Trial
- Animal models of anemia of inflammation: Methodological advances, limitations, and translational applications.Animal models and experimental medicine · 2026Review
- Halofuginone suppresses hepcidin by a heparan sulfate-dependent mechanism to treat iron disorders in mice.Blood advances · 2026Article
- Non-anticoagulant heparins: glycan-mediated immune modulation and therapeutic applications.Frontiers in immunology · 2026Review
- Current Landscape of Hepcidin Therapeutics.Advances in experimental medicine and biology · 2025Review
- Sevuparin strongly reduces hepcidin expression in cells, mice, and healthy human volunteers.HemaSphere · 2024Article
- Research advances on molecular mechanism and natural product therapy of iron metabolism in heart failure.European journal of medical research · 2024Review
- Anemia in patients receiving anticancer treatments: focus on novel therapeutic approaches.Frontiers in oncology · 2024Review
- Distinctive modulation of hepcidin in cancer and its therapeutic relevance.Frontiers in oncology · 2023Review
- Physiology and Inflammation Driven Pathophysiology of Iron Homeostasis-Mechanistic Insights into Anemia of Inflammation and Its Treatment.Nutrients · 2021Review
- ESA, Iron Therapy and New Drugs: Are There New Perspectives in the Treatment of Anaemia?Journal of clinical medicine · 2021Review
- Hepcidin Promoted Ferroptosis through Iron Metabolism which Is Associated with DMT1 Signaling Activation in Early Brain Injury following Subarachnoid Hemorrhage.Oxidative medicine and cellular longevity · 2021Article
- Review
- Inflammation Mediated Hepcidin-Ferroportin Pathway and Its Therapeutic Window in Breast Cancer.Breast cancer (Dove Medical Press) · 2020Review
- Host-Pathogen Interaction as a Novel Target for Host-Directed Therapies in Tuberculosis.Frontiers in immunology · 2020Review
- Iron metabolism and iron disorders revisited in the hepcidin era.Haematologica · 2020Review
- Therapeutic Advances in Regulating the Hepcidin/Ferroportin Axis.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Hepatic heparan sulfate is a master regulator of hepcidin expression and iron homeostasis in human hepatocytes and mice.The Journal of biological chemistry · 2019Article
- Hepcidin Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2018Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepcidin controls systemic iron availability, and its excess contributes to the anemia of chronic diseases, the most prevalent anemia in hospitalized patients. We previously reported that heparins are efficient hepcidin inhibitors both in vitro and in vivo, but their anticoagulant activity limits therapeutic use. We studied nonanticoagulant heparins produced by N-acetylation and oxidation/reduction (glycol-split) that lost antithrombin-binding affinity. Four nonanticoagulant heparins inhibited hepcidin expression in hepatic HepG2 cells and primary hepatocytes. The 2 most potent ones used in mice suppressed liver hepcidin expression and serum hepcidin in 6 hours, with a significant decrease of spleen iron. This occurred also in lipopolysaccharide (LPS)-treated animals that mimic inflammation, as well as after chronic 1-week treatments, without evident adverse effects on coagulation. Heparin injections increased iron mobilization and facilitated the recovery from the anemia induced by heat-killed Brucella abortus, a model of inflammatory anemia. The heparins were used also in Bmp6(-/-) mice. A single dose of heparin reduced the already low level of hepcidin of these mice and prevented its induction by LPS. These nonanticoagulant compounds impair bone morphogenetic protein /sons of mothers against decapentaplegic signaling with no evident adverse effect in vivo, even when administered chronically. They may offer a strategy for the treatment of diseases with high hepcidin levels.
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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.