ReviewMolecules (Basel, Switzerland)2017
Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia.
Review in Molecules (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed, 24 citations in OpenAlex.
- Non-anticoagulant heparins: glycan-mediated immune modulation and therapeutic applications.Frontiers in immunology · 2026Review
- Iron metabolism and management: focus on chronic kidney disease.Kidney international supplements · 2021Article
- Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage.Biomedicines · 2020Review
- Retinal Degeneration and Alzheimer's Disease: An Evolving Link.International journal of molecular sciences · 2020Review
- Prions and prion diseases: Insights from the eye.Experimental eye research · 2020Review
- TGFβ2-Hepcidin Feed-Forward Loop in the Trabecular Meshwork Implicates Iron in Glaucomatous Pathology.Investigative ophthalmology & visual science · 2020Article
- Local synthesis of hepcidin in the anterior segment of the eye: A novel observation with physiological and pathological implications.Experimental eye research · 2020Article
- Hepatic heparan sulfate is a master regulator of hepcidin expression and iron homeostasis in human hepatocytes and mice.The Journal of biological chemistry · 2019Article
- Looking Forward to the Future of Heparin: New Sources, Developments and Applications.Molecules (Basel, Switzerland) · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The peptide hormone hepcidin is a key controller of systemic iron homeostasis, and its expression in the liver is mainly regulated by bone morphogenetic proteins (BMPs), which are heparin binding proteins. In fact, heparins are strong suppressors of hepcidin expression in hepatic cell lines that act by inhibiting the phosphorylation of SMAD1/5/8 proteins elicited by the BMPs. The inhibitory effect of heparins has been demonstrated in cells and in mice, where subcutaneous injections of non-anticoagulant heparins inhibited liver hepcidin expression and increased iron bioavailability. The chemical characteristics for high anti-hepcidin activity in vitro and in vivo include the 2O-and 6O-sulfation and a molecular weight above 7 kDa. The most potent heparins have been found to be the super-sulfated ones, active in hepcidin suppression with a molecular weight as low as 4 kDa. Moreover, the alteration of endogenous heparan sulfates has been found to cause a reduction in hepcidin expression in vitro and in vivo, indicating that heparins act by interfering with the interaction between BMPs and components of the complex involved in the activation of the BMP/SMAD1/5/8 pathway. This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.
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