Evidence map›Paper›PMID 31387234›Full record

ReviewMedicines (Basel, Switzerland)2019

A Short Review of Iron Metabolism and Pathophysiology of Iron Disorders.

Andronicos Yiannikourides, Gladys O Latunde-Dada

Open access · goldAbstract readReview
In one paragraph

Review in Medicines (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
14.1field-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

114 citing papers in PubMed, 239 citations in OpenAlex.

  1. Trial
  2. Metallothionein and neurodegenerative diseases.Neural regeneration research · 2026
    Article
  3. A review - Prescribing iron salts: Comparison of efficacy and tolerance of different iron complexes.South African family practice : official journal of the South African Academy of Family Practice/Primary Care · 2026
    Review
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54 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.

Andronicos YiannikouridesFaculty of Life Sciences and Medicine, Henriette Raphael House Guy's Campus King's College London, London SE1 1UL, UK.
Gladys O Latunde-DadaDepartment of Nutritional Sciences, School of Life Course Sciences, King's College London, Franklin-Wilkins-Building, 150 Stamford Street, London SE1 9NH, UK. yemisi.latunde-dada@kcl.ac.uk.ORCID 0000-0002-0607-6909
King's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron is a vital trace element for humans, as it plays a crucial role in oxygen transport, oxidative metabolism, cellular proliferation, and many catalytic reactions. To be beneficial, the amount of iron in the human body needs to be maintained within the ideal range. Iron metabolism is one of the most complex processes involving many organs and tissues, the interaction of which is critical for iron homeostasis. No active mechanism for iron excretion exists. Therefore, the amount of iron absorbed by the intestine is tightly controlled to balance the daily losses. The bone marrow is the prime iron consumer in the body, being the site for erythropoiesis, while the reticuloendothelial system is responsible for iron recycling through erythrocyte phagocytosis. The liver has important synthetic, storing, and regulatory functions in iron homeostasis. Among the numerous proteins involved in iron metabolism, hepcidin is a liver-derived peptide hormone, which is the master regulator of iron metabolism. This hormone acts in many target tissues and regulates systemic iron levels through a negative feedback mechanism. Hepcidin synthesis is controlled by several factors such as iron levels, anaemia, infection, inflammation, and erythropoietic activity. In addition to systemic control, iron balance mechanisms also exist at the cellular level and include the interaction between iron-regulatory proteins and iron-responsive elements. Genetic and acquired diseases of the tissues involved in iron metabolism cause a dysregulation of the iron cycle. Consequently, iron deficiency or excess can result, both of which have detrimental effects on the organism.

Indexed as

anemiadisordershepcidinIronmetabolism

Identifiers

PMID31387234
PMCPMC6789448
OpenAlexW2964465172

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.