Evidence map›Paper›PMID 30401708›Full record

ReviewBlood2019

Liver iron sensing and body iron homeostasis.

Chia-Yu Wang, Jodie L Babitt

Open access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed, 3 pooled it
15.3field-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

185 citing papers in PubMed, 3 syntheses or guidelines pooled it, 351 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. The neogenin-hemojuvelin axis in murine liver is crucial for hepcidin expression.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Iron Overload: Pathophysiology, Diagnosis and Monitoring.International journal of laboratory hematology · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Kupffer cells: Orchestrators of liver physiology.Liver research (Beijing, China) · 2026
    Review
  18. Article
  19. Review
  20. Article

125 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.

Chia-Yu WangDivision of Nephrology, Program in Membrane Biology, Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0003-3679-6453
Jodie L BabittDivision of Nephrology, Program in Membrane Biology, Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA babitt.jodie@mgh.harvard.edu.ORCID 0000-0003-1228-1551
Harvard University · US

Funding

Regulation of Iron Homeostasis by BMP SignalingR01DK087727 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BABITT, JODIE L · 2010 to 2024
$6.0M
NIDDK NIH HHS R01 DK087727
6 · The paper itself

Abstract

The liver orchestrates systemic iron balance by producing and secreting hepcidin. Known as the iron hormone, hepcidin induces degradation of the iron exporter ferroportin to control iron entry into the bloodstream from dietary sources, iron recycling macrophages, and body stores. Under physiologic conditions, hepcidin production is reduced by iron deficiency and erythropoietic drive to increase the iron supply when needed to support red blood cell production and other essential functions. Conversely, hepcidin production is induced by iron loading and inflammation to prevent the toxicity of iron excess and limit its availability to pathogens. The inability to appropriately regulate hepcidin production in response to these physiologic cues underlies genetic disorders of iron overload and deficiency, including hereditary hemochromatosis and iron-refractory iron deficiency anemia. Moreover, excess hepcidin suppression in the setting of ineffective erythropoiesis contributes to iron-loading anemias such as β-thalassemia, whereas excess hepcidin induction contributes to iron-restricted erythropoiesis and anemia in chronic inflammatory diseases. These diseases have provided key insights into understanding the mechanisms by which the liver senses plasma and tissue iron levels, the iron demand of erythrocyte precursors, and the presence of potential pathogens and, importantly, how these various signals are integrated to appropriately regulate hepcidin production. This review will focus on recent insights into how the liver senses body iron levels and coordinates this with other signals to regulate hepcidin production and systemic iron homeostasis.

Indexed as

HomeostasisHumansIronIron Metabolism DisordersLiverIron

Identifiers

PMID30401708
PMCPMC6318427
OpenAlexW2899671176

What OpenQuestion holds

Textmetadata
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.