Evidence map›Paper›PMID 31504675›Full record

ReviewThe Journal of nutrition2019

Animal Models of Normal and Disturbed Iron and Copper Metabolism.

Xiaoyu Wang, Michael D Garrick, James F Collins

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of nutrition, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Putative Animal Models of Restless Legs Syndrome: A Systematic Review and Evaluation of Their Face and Construct Validity.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Pooled it
  2. Cuproptosis in iron overload hepatocytes.Cell death & disease · 2026
    Article
  3. Cuproptosis: potential new direction in liver-related diseases research and treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. 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

3 authors at 2 institutions in 1 country.

Xiaoyu WangFood Science and Human Nutrition Department, University of Florida, Gainesville, FL, USA.
Michael D GarrickDepartment of Biochemistry, University at Buffalo-The State University of New York, Buffalo, NY, USA.
James F CollinsFood Science and Human Nutrition Department, University of Florida, Gainesville, FL, USA.
University of Florida · USUniversity at Buffalo, State University of New York · US

Funding

Molecular Mechanisms of Intestinal Metal Ion Transport During Iron-DeficiencyR01DK074867 · NIDDK · UNIVERSITY OF FLORIDA · PI COLLINS, JAMES F., VIDYASAGAR, SADASIVAN · 2007 to 2022
$5.1M
Divalent Metal-ion Transporter 1 as a Therapeutic Target to Optimize Intestinal Iron TransportR01DK109717 · NIDDK · UNIVERSITY OF FLORIDA · PI COLLINS, JAMES F. · 2016 to 2020
$2.6M
NIDDK NIH HHS R01 DK074867NIDDK NIH HHS R01 DK109717
6 · The paper itself

Abstract

Research on the interplay between iron and copper metabolism in humans began to flourish in the mid-20th century, and diseases associated with dysregulated homeostasis of these essential trace minerals are common even today. Iron deficiency is the most frequent cause of anemia worldwide, leading to significant morbidity, particularly in developing countries. Iron overload is also quite common, usually being the result of genetic mutations which lead to inappropriate expression of the iron-regulatory hormone hepcidin. Perturbations of copper homeostasis in humans have also been described, including rare genetic conditions which lead to severe copper deficiency (Menkes disease) or copper overload (Wilson disease). Historically, the common laboratory rat (Rattus norvegicus) was the most frequently utilized species to model human physiology and pathophysiology. Recently, however, the development of genetic-engineering technology combined with the worldwide availability of numerous genetically homogenous (i.e., inbred) mouse strains shifted most research on iron and copper metabolism to laboratory mice. This created new opportunities to understand the function of individual genes in the context of a living animal, but thoughtful consideration of whether mice are the most appropriate models of human pathophysiology was not necessarily involved. Given this background, this review is intended to provide a guide for future research on iron- and copper-related disorders in humans. Generation of complementary experimental models in rats, swine, and other mammals is now facile given the advent of newer genetic technologies, thus providing the opportunity to accelerate the identification of pathogenic mechanisms and expedite the development of new treatments to mitigate these important human disorders.

Indexed as

Models, AnimalAnemia, Iron-DeficiencyAnimalsCopperDietIronCopperIronanemiacopper deficiencyhepcidinhereditary hemochromatosisiron deficiencyiron-deficiency anemiaMenkes diseaseWilson diseaseβ-thalassemia

Identifiers

PMID31504675
PMCPMC6887953
OpenAlexW2969371715

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.