Evidence map›Paper›PMID 25970748›Full record

ArticleScientific reports2015

ROS-mediated iron overload injures the hematopoiesis of bone marrow by damaging hematopoietic stem/progenitor cells in mice.

Xiao Chai, Deguan Li, Xiaoli Cao, Yuchen Zhang, Juan Mu, Wenyi Lu, Xia Xiao, Chengcheng Li, Juanxia Meng, Jie Chen and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 140 citations in OpenAlex.

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  5. Iron overload induced by ferric derisomaltose and ferric carboxymaltose both increase FGF-23 levels and lead to osteomalacia and bone loss in normal mice.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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  19. Role of reactive oxygen species in myelodysplastic syndromes.Cellular & molecular biology letters · 2024
    Review
  20. Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Xiao Chai1] Department of Hematology, Tianjin First Central Hospital, Tianjin 300192, China [2] Department of Hematology, The Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China.
Deguan LiTianjin Key Lab of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Academy of Medical Science and Peking Union Medical College, Tianjin 300192, China.
Xiaoli CaoDepartment of Hematology, Tianjin First Central Hospital, Tianjin 300192, China.
Yuchen ZhangDepartment of Hematology, Tianjin First Central Hospital, Tianjin 300192, China.
Juan MuDepartment of Hematology, Tianjin First Central Hospital, Tianjin 300192, China.
Wenyi LuDepartment of Hematology, Tianjin First Central Hospital, Tianjin 300192, China.
Xia XiaoDepartment of Hematology, Tianjin First Central Hospital, Tianjin 300192, China.
Chengcheng LiTianjin Key Lab of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Academy of Medical Science and Peking Union Medical College, Tianjin 300192, China.
Juanxia MengDepartment of Hematology, Tianjin First Central Hospital, Tianjin 300192, China.
Jie ChenDepartment of Hematology, Tianjin First Central Hospital, Tianjin 300192, China.
Qing LiDepartment of Hematology, Tianjin First Central Hospital, Tianjin 300192, China.
Jishi WangDepartment of Hematology, The Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China.
Aimin MengTianjin Key Lab of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Academy of Medical Science and Peking Union Medical College, Tianjin 300192, China.
Mingfeng ZhaoDepartment of Hematology, Tianjin First Central Hospital, Tianjin 300192, China.
Tianjin Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNTianjin First Center Hospital · CNAffiliated Hospital of Guizhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron overload, caused by hereditary hemochromatosis or repeated blood transfusions in some diseases, such as beta thalassemia, bone marrow failure and myelodysplastic syndrome, can significantly induce injured bone marrow (BM) function as well as parenchyma organ dysfunctions. However, the effect of iron overload and its mechanism remain elusive. In this study, we investigated the effects of iron overload on the hematopoietic stem and progenitor cells (HSPCs) from a mouse model. Our results showed that iron overload markedly decreased the ratio and clonogenic function of murine HSPCs by the elevation of reactive oxygen species (ROS). This finding is supported by the results of NAC or DFX treatment, which reduced ROS level by inhibiting NOX4 and p38MAPK and improved the long-term and multi-lineage engrafment of iron overload HSCs after transplantation. Therefore, all of these data demonstrate that iron overload injures the hematopoiesis of BM by enhancing ROS through NOX4 and p38MAPK. This will be helpful for the treatment of iron overload in patients with hematopoietic dysfunction.

Indexed as

HematopoiesisAnimalsBone MarrowBone Marrow CellsBone Marrow TransplantationColony-Forming Units AssayDisease Models, AnimalGraft SurvivalHematopoiesis, ExtramedullaryHematopoietic Stem CellsIron OverloadMaleMiceNADPH Oxidase 4NADPH Oxidasesp38 Mitogen-Activated Protein KinasesNADPH Oxidase 4NADPH OxidasesNox4 protein, mousep38 Mitogen-Activated Protein KinasesReactive Oxygen Species

Identifiers

PMID25970748
PMCPMC4429544
OpenAlexW2266818917

What OpenQuestion holds

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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.