Evidence map›Paper›PMID 30857202›Full record

ArticleCells2019

Excessive Reactive Iron Impairs Hematopoiesis by Affecting Both Immature Hematopoietic Cells and Stromal Cells.

Hirokazu Tanaka, J Luis Espinoza, Ryosuke Fujiwara, Shinya Rai, Yasuyoshi Morita, Takashi Ashida, Yuzuru Kanakura, Itaru Matsumura

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Role of reactive oxygen species in myelodysplastic syndromes.Cellular & molecular biology letters · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. The Role of Iron in Benign and Malignant Hematopoiesis.Antioxidants & redox signaling · 2021
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. 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

8 authors at 2 institutions in 1 country.

Hirokazu TanakaDepartment of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama 589-8511, Japan. htanaka@med.kindai.ac.jp.ORCID 0000-0002-7192-525X
J Luis EspinozaDepartment of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama 589-8511, Japan. luis@med.kindai.ac.jp.ORCID 0000-0002-1794-6666
Ryosuke FujiwaraDepartment of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama 589-8511, Japan. r-fujiwara@med.kindai.ac.jp.
Shinya RaiDepartment of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama 589-8511, Japan. rai@med.kindai.ac.jp.ORCID 0000-0003-3929-9751
Yasuyoshi MoritaDepartment of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama 589-8511, Japan. moriyasu@med.kindai.ac.jp.
Takashi AshidaDepartment of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama 589-8511, Japan. ashida@med.kindai.ac.jp.
Yuzuru KanakuraDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan. kanakura@bldon.med.osaka-u.ac.jp.
Itaru MatsumuraDepartment of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama 589-8511, Japan. i.matsu@med.kindai.ac.jp.
Kindai University · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron overload is the accumulation of excess iron in the body that may occur as a result of various genetic disorders or as a consequence of repeated blood transfusions. The surplus iron is then stored in the liver, pancreas, heart and other organs, which may lead to chronic liver disease or cirrhosis, diabetes and heart disease, respectively. In addition, excessive iron may impair hematopoiesis, although the mechanisms of this deleterious effect is not entirely known. In this study, we found that ferrous ammonium sulfate (FeAS), induced growth arrest and apoptosis in immature hematopoietic cells, which was mediated via reactive oxygen species (ROS) activation of p38MAPK and JNK pathways. In in vitro hematopoiesis derived from embryonic stem cells (ES cells), FeAS enhanced the development of dysplastic erythroblasts but inhibited their terminal differentiation; in contrast, it had little effect on the development of granulocytes, megakaryocytes, and B lymphocytes. In addition to its directs effects on hematopoietic cells, iron overload altered the expression of several adhesion molecules on stromal cells and impaired the cytokine production profile of these cells. Therefore, excessive iron would affect whole hematopoiesis by inflicting vicious effects on both immature hematopoietic cells and stromal cells.

Indexed as

AnimalsApoptosisBone Marrow CellsCell Adhesion MoleculesCell Cycle CheckpointsCell DifferentiationCell LineCell LineageErythroid CellsFerrous CompoundsHematopoiesisHematopoietic Stem CellsIronMacrophagesMegakaryocytesMice, Inbred C57BLammonium ferrous sulfateCell Adhesion MoleculesFerrous CompoundsIronQuaternary Ammonium CompoundsReactive Oxygen Specieshematopoiesishematopoietic stem cellsiron overloadoxidative stressstromal cells

Identifiers

PMID30857202
PMCPMC6468739
OpenAlexW2921806030

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.