Evidence map›Paper›PMID 29719207›Full record

ReviewFree radical biology & medicine2018

The intricate role of selenium and selenoproteins in erythropoiesis.

Chang Liao, Bradley A Carlson, Robert F Paulson, K Sandeep Prabhu

Abstract readReview
In one paragraph

Review in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Redox Modulation of Erythropoiesis by Selenoproteins.Biological trace element research · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Human Genetic Disorders Resulting in Systemic Selenoprotein Deficiency.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Chang LiaoDepartment of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, PA 16802, USA.
Bradley A CarlsonMolecular Biology of Selenium Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Robert F PaulsonDepartment of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, PA 16802, USA. Electronic address: rfp5@psu.edu.
K Sandeep PrabhuDepartment of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, PA 16802, USA. Electronic address: ksp4@psu.edu.
Pennsylvania State University · USNational Institutes of Health · US

Funding

The BMP4 dependent stress erythropoiesis pathway in short-term radioprotectionR01DK080040 · NIDDK · PENNSYLVANIA STATE UNIVERSITY, THE · PI PAULSON, ROBERT FRANK · 2009 to 2017
$2.6M
Cellular Selenium Status and PGJ2 Metabolism (PA-17-078 supplement 2017)R01DK077152 · NIDDK · PENNSYLVANIA STATE UNIVERSITY, THE · PI PRABHU, KUMBLE SANDEEP · 2008 to 2018
$2.5M
NIDDK NIH HHS R01 DK077152NIDDK NIH HHS R01 DK080040
6 · The paper itself

Abstract

Selenium (Se) is incorporated as the 21st amino acid selenocysteine (Sec) into the growing polypeptide chain of proteins involved in redox gatekeeper functions. Erythropoiesis presents a particular problem to redox regulation as the presence of iron, heme, and unpaired globin chains lead to high levels of free radical-mediated oxidative stress, which are detrimental to erythroid development and can lead to anemia. Under homeostatic conditions, bone marrow erythropoiesis produces sufficient erythrocytes to maintain homeostasis. In contrast, anemic stress induces an alternative pathway, stress erythropoiesis, which rapidly produces new erythrocytes at extramedullary sites, such as spleen, to alleviate anemia. Previous studies suggest that dietary Se protects erythrocytes from such oxidative damage and the absence of selenoproteins causes hemolysis of erythrocytes due to oxidative stress. Furthermore, Se deficiency or lack of selenoproteins severely impairs stress erythropoiesis exacerbating the anemia in rodent models and human patients. Interestingly, erythroid progenitors develop in close proximity with macrophages in structures referred to as erythroblastic islands (EBIs), where macrophage expression of selenoproteins appears to be critical for the expression of heme transporters to facilitate export of heme from macrophage stores to the developing erythroid cells. Here we review the role of Se and selenoproteins in the intrinsic development of erythroid cells in addition to their role in the development of the erythropoietic niche that supports the functional role of EBIs in erythroid expansion and maturation in the spleen during recovery from anemia.

Indexed as

AnemiaAnimalsCell DifferentiationErythroblastsErythropoiesisHumansMacrophagesOxidation-ReductionOxidative StressSeleniumSelenoproteinsSeleniumSelenoproteinsErythroblastic islandsHemeMacrophagesStress erythropoiesis

Identifiers

PMID29719207
PMCPMC6168382
OpenAlexW2802073596

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.