Evidence map›Paper›PMID 29981834›Full record

ReviewFree radical biology & medicine2019

Erythropoietic regulators of iron metabolism.

Tomas Ganz

Abstract readReview
In one paragraph

Review in Free radical biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
13.2field-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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.

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10 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

1 author at 1 institution in 1 country.

Tomas GanzDepartments of Medicine and Pathology, David Geffen School of Medicine, UCLA, Los Angeles, USA. Electronic address: tganz@mednet.ucla.edu.
University of California, Los Angeles · US

Funding

The role of erythroferrone in iron homeostasis and in iron-loading anemiasR01DK065029 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GANZ, TOMAS · 2004 to 2017
$4.9M
NIDDK NIH HHS R01 DK065029
6 · The paper itself

Abstract

Erythropoiesis is the predominant consumer of iron in humans and other vertebrates. By decreasing the transcription of the gene encoding the iron-regulatory hormone hepcidin, erythropoietic activity stimulates iron absorption, as well as the release of iron from recycling macrophages and from stores in hepatocytes. The main erythroid regulator of hepcidin is erythroferrone (ERFE), synthesized and secreted by erythroblasts in the marrow and extramedullary sites. The production of ERFE is induced by erythropoietin (EPO) and is also proportional to the total number of responsive erythroblasts. ERFE acts on hepatocytes to suppress the production of hepcidin, through an as yet unknown mechanism that involves the bone morphogenetic protein pathway. By suppressing hepcidin, ERFE facilitates iron delivery during stress erythropoiesis but also contributes to iron overload in anemias with ineffective erythropoiesis. Although most of these mechanisms have been defined in mouse models, studies to date indicate that the pathophysiology of ERFE is similar in humans. ERFE antagonists and mimics may prove useful for the prevention and treatment of iron disorders.

Indexed as

AnemiaBone Morphogenetic ProteinsErythropoiesisErythropoietinHepatocytesHepcidinsHumansIronIron OverloadMacrophagesPeptide HormonesBone Morphogenetic ProteinsErfe protein, humanErythropoietinHepcidinsIronPeptide HormonesAnemiaErythroferroneErythropoiesisHepcidinIron

Identifiers

PMID29981834
PMCPMC6320727
OpenAlexW2835234069

What OpenQuestion holds

Textmetadata
LicenceTDM
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.