Evidence map›Paper›PMID 25622253›Full record

ReviewInternational journal of molecular sciences2015

Oxidative stress, bone marrow failure, and genome instability in hematopoietic stem cells.

Christine Richardson, Shan Yan, C Greer Vestal

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–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

41 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Review
  7. Modulation of Redox Metabolism, CD147, and CD47 Expression with the Maturation of Hematopoietic Stem Cells in Bone Marrow.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. The MicroalgaMolecules (Basel, Switzerland) · 2022
    Article
  16. Article
  17. Article
  18. Autophagy and Metabolism in Normal and Malignant Hematopoiesis.International journal of molecular sciences · 2021
    Review
  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

3 authors.

Christine RichardsonDepartment of Biological Sciences, UNC Charlotte, 9201 University City Blvd., Woodward Hall Room 386B, Charlotte, NC 28223, USA. c.richardson@uncc.edu.
Shan YanDepartment of Biological Sciences, UNC Charlotte, 9201 University City Blvd., Woodward Hall Room 386B, Charlotte, NC 28223, USA. shan.yan@uncc.edu.
C Greer VestalDepartment of Biological Sciences, UNC Charlotte, 9201 University City Blvd., Woodward Hall Room 386B, Charlotte, NC 28223, USA. cvestal1@uncc.edu.

Funding

Etiology of Translocations in Hematopoietic CellsR01CA100159 · NCI · UNIVERSITY OF NORTH CAROLINA CHARLOTTE · PI RICHARDSON, CHRISTINE A. · 2003 to 2017
$2.4M
Role of TopBP1 partner WDR18 in DNA damage checkpoint and DNA replicationR15GM101571 · NIGMS · UNIVERSITY OF NORTH CAROLINA CHARLOTTE · PI YAN, SHAN · 2012 to 2012
$297k
NCI NIH HHS R01 CA100159NIGMS NIH HHS R15 GM101571
6 · The paper itself

Abstract

Reactive oxygen species (ROS) can be generated by defective endogenous reduction of oxygen by cellular enzymes or in the mitochondrial respiratory pathway, as well as by exogenous exposure to UV or environmental damaging agents. Regulation of intracellular ROS levels is critical since increases above normal concentrations lead to oxidative stress and DNA damage. A growing body of evidence indicates that the inability to regulate high levels of ROS leading to alteration of cellular homeostasis or defective repair of ROS-induced damage lies at the root of diseases characterized by both neurodegeneration and bone marrow failure as well as cancer. That these diseases may be reflective of the dynamic ability of cells to respond to ROS through developmental stages and aging lies in the similarities between phenotypes at the cellular level. This review summarizes work linking the ability to regulate intracellular ROS to the hematopoietic stem cell phenotype, aging, and disease.

Indexed as

Oxidative StressAnemia, AplasticAnimalsBone Marrow DiseasesBone Marrow Failure DisordersDNA DamageDNA RepairGenomic InstabilityHematopoietic Stem CellsHemoglobinuria, ParoxysmalHumansReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID25622253
PMCPMC4346841

What Socratic 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 Socratic graph.