Evidence map›Paper›PMID 28096133›Full record

ReviewAdvances in nutrition (Bethesda, Md.)2017

Regulation of the Iron Homeostatic Hormone Hepcidin.

Veena Sangkhae, Elizabeta Nemeth

Open access · bronzeAbstract readReview
In one paragraph

Review in Advances in nutrition (Bethesda, Md.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 232 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
232citing papers in PubMed, 2 pooled it
22.3field-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

232 citing papers in PubMed, 2 syntheses or guidelines pooled it, 423 citations in OpenAlex.

  1. Pooled it
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  11. Dysregulated iron metabolism in remodeling of aging asthmatic human airways.American journal of physiology. Cell physiology · 2026
    Article
  12. Genes · 2026
    Article
  13. Article
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  16. Cortisol Stress Response is Associated with Iron Status in Pregnancy.medRxiv : the preprint server for health sciences · 2026
    Article
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  20. Review

172 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.

Veena SangkhaeCenter for Iron Disorders, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA.
Elizabeta NemethCenter for Iron Disorders, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA enemeth@mednet.ucla.edu.
University of California, Los Angeles · US

Funding

UCLA Pulmonary and Critical Care Medicine Training ProgramT32HL072752 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI JOHN A BELPERIO, TOMAS GANZ · 2003 to 2026
$8.3M
Ferroportin Structure and functionR01DK107309 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI JORMAKKA, MIKA, MACKENZIE, BRYAN · 2015 to 2019
$3.0M
NHLBI NIH HHS T32 HL072752NIDDK NIH HHS R01 DK107309
6 · The paper itself

Abstract

Iron is required for many biological processes but is also toxic in excess; thus, body iron balance is maintained through sophisticated regulatory mechanisms. The lack of a regulated iron excretory mechanism means that body iron balance is controlled at the level of absorption from the diet. Iron absorption is regulated by the hepatic peptide hormone hepcidin. Hepcidin also controls iron release from cells that recycle or store iron, thus regulating plasma iron concentrations. Hepcidin exerts its effects through its receptor, the cellular iron exporter ferroportin. Important regulators of hepcidin, and therefore of systemic iron homeostasis, include plasma iron concentrations, body iron stores, infection and inflammation, and erythropoiesis. Disturbances in the regulation of hepcidin contribute to the pathogenesis of many iron disorders: hepcidin deficiency causes iron overload in hereditary hemochromatosis and nontransfused β-thalassemia, whereas overproduction of hepcidin is associated with iron-restricted anemias seen in patients with chronic kidney disease, chronic inflammatory diseases, some cancers, and inherited iron-refractory iron deficiency anemia. This review summarizes our current understanding of the molecular mechanisms and signaling pathways involved in the control of hepcidin synthesis in the liver, a principal determinant of plasma hepcidin concentrations.

Indexed as

HomeostasisAnemia, Iron-DeficiencyAnimalsCation Transport ProteinsDisease Models, AnimalErythropoiesisFerroportinHemochromatosisHepcidinsHumansInflammationIronIron DeficienciesIron OverloadLiverSignal TransductionCation Transport ProteinsFerroportinHepcidinsIronanemiaerythropoiesishepcidininflammationiron

Identifiers

PMID28096133
PMCPMC5227985
OpenAlexW2575751745

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.