Evidence map›Paper›PMID 30215866›Full record

ReviewComprehensive Physiology2018

Intersection of Iron and Copper Metabolism in the Mammalian Intestine and Liver.

Caglar Doguer, Jung-Heun Ha, James F Collins

Abstract readReview
In one paragraph

Review in Comprehensive Physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

109 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Copper, cuproptosis, and cancer: biology concepts of a novel cell death.Apoptosis : an international journal on programmed cell death · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Metallothionein and neurodegenerative diseases.Neural regeneration research · 2026
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
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49 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

3 authors at 2 institutions in 3 countries.

Caglar DoguerFood Science and Human Nutrition Department, University of Florida, Florida, Gainesville, USA.
Jung-Heun HaFood Science and Human Nutrition Department, University of Florida, Florida, Gainesville, USA.
James F CollinsFood Science and Human Nutrition Department, University of Florida, Florida, Gainesville, USA.
University of Florida · USNamık Kemal University · TR

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

Iron and copper have similar physiochemical properties; thus, physiologically relevant interactions seem likely. Indeed, points of intersection between these two essential trace minerals have been recognized for many decades, but mechanistic details have been lacking. Investigations in recent years have revealed that copper may positively influence iron homeostasis, and also that iron may antagonize copper metabolism. For example, when body iron stores are low, copper is apparently redistributed to tissues important for regulating iron balance, including enterocytes of upper small bowel, the liver, and blood. Copper in enterocytes may positively influence iron transport, and hepatic copper may enhance biosynthesis of a circulating ferroxidase, ceruloplasmin, which potentiates iron release from stores. Moreover, many intestinal genes related to iron absorption are transactivated by a hypoxia-inducible transcription factor, hypoxia-inducible factor-2α (HIF2α), during iron deficiency. Interestingly, copper influences the DNA-binding activity of the HIF factors, thus further exemplifying how copper may modulate intestinal iron homeostasis. Copper may also alter the activity of the iron-regulatory hormone hepcidin. Furthermore, copper depletion has been noted in iron-loading disorders, such as hereditary hemochromatosis. Copper depletion may also be caused by high-dose iron supplementation, raising concerns particularly in pregnancy when iron supplementation is widely recommended. This review will cover the basic physiology of intestinal iron and copper absorption as well as the metabolism of these minerals in the liver. Also considered in detail will be current experimental work in this field, with a focus on molecular aspects of intestinal and hepatic iron-copper interplay and how this relates to various disease states. © 2018 American Physiological Society. Compr Physiol 8:1433-1461, 2018.

Indexed as

AnimalsCopperHumansIntestinal AbsorptionIntestinal MucosaIronLiverMetalloproteinsCopperIronMetalloproteins

Identifiers

PMID30215866
PMCPMC6460475
OpenAlexW2902666242

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.