Evidence map›Paper›PMID 34027264›Full record

ReviewHepatology communications2021

Hepcidin Signaling in Health and Disease: Ironing Out the Details.

Kris V Kowdley, Eric M Gochanour, Vinay Sundaram, Raj A Shah, Priya Handa

Open access · goldAbstract readReview
In one paragraph

Review in Hepatology communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 84 citations in OpenAlex.

  1. Cuproptosis in iron overload hepatocytes.Cell death & disease · 2026
    Article
  2. Article
  3. Review
  4. Haemochromatosis - a modern clinician's guide.Internal medicine journal · 2026
    Review
  5. Review
  6. Low 5HTJournal of neurochemistry · 2026
    Review
  7. Review
  8. Iron-Based Nanoparticles as Delivery Tools.Pharmaceuticals (Basel, Switzerland) · 2026
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
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

5 authors at 4 institutions in 1 country.

Kris V KowdleyLiver Institute Northwest and Elson S. Floyd College of MedicineWashington State UniversitySpokaneWAUSA.ORCID 0000-0002-8553-3652
Eric M GochanourLiver Institute Northwest and Elson S. Floyd College of MedicineWashington State UniversitySpokaneWAUSA.
Vinay SundaramDivision of Gastroenterology and Comprehensive Transplant CenterLos AngelesCAUSA.ORCID 0000-0002-1450-7756
Raj A ShahLiver Care Network and Organ Care ResearchSwedish Medical CenterSeattleWAUSA.
Priya HandaLiver Care Network and Organ Care ResearchSwedish Medical CenterSeattleWAUSA.
Swedish Medical Center · USComprehensive Cardiovascular · USLiver Institute Northwest · USWashington State University Spokane · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepcidin, a peptide hormone produced by hepatocytes, is the central regulator of systemic iron homeostasis through its interaction with ferroportin, the major cellular iron export protein. Hepcidin binding to ferroportin results in reduced iron export from macrophages and intestinal absorptive cells, leading to decreased serum iron levels. Hepcidin expression is influenced by several factors that include serum and liver iron stores, erythropoiesis, hypoxia, inflammation, and infection. Erythropoietic drive and hypoxia suppress hepcidin expression and promote red cell production. In contrast, inflammation and infection are associated with increased hepcidin production to sequester iron intracellularly as a means of depriving microorganisms of iron. Chronic inflammation may up-regulate hepcidin expression through the interleukin-6 (IL-6)-Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) pathway. The bone morphogenetic protein (BMP)-mothers against decapentaplegic homolog (SMAD) pathway is a major positive driver of hepcidin expression in response to either increased circulating iron in the form of transferrin or iron loading in organs. Hereditary hemochromatosis (HH) consists of several inherited disorders that cause inappropriately reduced hepcidin expression in response to body iron stores, leading to increased iron absorption from a normal diet. The most common form of HH is due to a mutation in the

Identifiers

PMID34027264
PMCPMC8122377
OpenAlexW3148770953

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.