Evidence map›Paper›PMID 34204327›Full record

ReviewInternational journal of molecular sciences2021

Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis.

Elizabeta Nemeth, Tomas Ganz

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 310 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
310citing papers in PubMed, 2 pooled it
44.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

310 citing papers in PubMed, 2 syntheses or guidelines pooled it, 482 citations in OpenAlex.

  1. Pooled it
  2. Daily oral iron supplementation during pregnancy.The Cochrane database of systematic reviews · 2024
    Pooled it
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Review
  8. Review
  9. Iron dysregulation in the central nervous system: implications for autism spectrum disorder.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. A review of the iron requirements and its determination in commercial poultry.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026
    Review
  17. Review
  18. Article
  19. Article
  20. Review

250 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Elizabeta NemethDepartment of Medicine, University of California, Los Angeles, CA 90095, USA.
Tomas GanzDepartments of Medicine and Pathology, University of California, Los Angeles, CA 90095, USA.
University of California, Los Angeles · US

Funding

Iron physiology and pathology in pregnancyR01HD096863 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI NEMETH, ELIZABETA · 2019 to 2023
$2.1M
NICHD NIH HHS R01 HD096863
6 · The paper itself

Abstract

Despite its abundance in the environment, iron is poorly bioavailable and subject to strict conservation and internal recycling by most organisms. In vertebrates, the stability of iron concentration in plasma and extracellular fluid, and the total body iron content are maintained by the interaction of the iron-regulatory peptide hormone hepcidin with its receptor and cellular iron exporter ferroportin (SLC40a1). Ferroportin exports iron from duodenal enterocytes that absorb dietary iron, from iron-recycling macrophages in the spleen and the liver, and from iron-storing hepatocytes. Hepcidin blocks iron export through ferroportin, causing hypoferremia. During iron deficiency or after hemorrhage, hepcidin decreases to allow iron delivery to plasma through ferroportin, thus promoting compensatory erythropoiesis. As a host defense mediator, hepcidin increases in response to infection and inflammation, blocking iron delivery through ferroportin to blood plasma, thus limiting iron availability to invading microbes. Genetic diseases that decrease hepcidin synthesis or disrupt hepcidin binding to ferroportin cause the iron overload disorder hereditary hemochromatosis. The opposite phenotype, iron restriction or iron deficiency, can result from genetic or inflammatory overproduction of hepcidin.

Indexed as

HomeostasisAnimalsAutocrine CommunicationBiological TransportCation Transport ProteinsDisease SusceptibilityFerroportinHepcidinsHumansIronLigandsMetabolic Networks and PathwaysParacrine CommunicationProtein BindingSignal TransductionTissue DistributionCation Transport ProteinsFerroportinHepcidinsIronLigandsanemiahemochromatosisiron deficiencyiron overloadmetal transport

Identifiers

PMID34204327
PMCPMC8235187
OpenAlexW3172506357

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.