Evidence map›Paper›PMID 25578474›Full record

ArticleLeukemia2015

HIF-1α is required for hematopoietic stem cell mobilization and 4-prolyl hydroxylase inhibitors enhance mobilization by stabilizing HIF-1α.

C E Forristal, B Nowlan, R N Jacobsen, V Barbier, G Walkinshaw, C R Walkley, I G Winkler, J P Levesque

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 16% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Review
  5. Real-ambient PMParticle and fibre toxicology · 2025
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  19. Review
  20. Role of HIF1International journal of stem cells · 2019
    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 4 institutions in 2 countries.

C E ForristalBlood and Bone Diseases Program, Mater Research Institute, University of Queensland, Woolloongabba, Queensland, Australia.
B NowlanBlood and Bone Diseases Program, Mater Research Institute, University of Queensland, Woolloongabba, Queensland, Australia.
R N Jacobsen1] Blood and Bone Diseases Program, Mater Research Institute, University of Queensland, Woolloongabba, Queensland, Australia [2] School of Medicine, University of Queensland, Brisbane, Queensland, Australia.
V BarbierBlood and Bone Diseases Program, Mater Research Institute, University of Queensland, Woolloongabba, Queensland, Australia.
G WalkinshawFibrogen Inc., San Francisco, CA, USA.
C R WalkleyStem Cell Regulation Unit, St Vincent's Institute and University of Melbourne, St Vincent's Hospital, Fitzroy, Victoria, Australia.
I G WinklerBlood and Bone Diseases Program, Mater Research Institute, University of Queensland, Woolloongabba, Queensland, Australia.
J P Levesque1] Blood and Bone Diseases Program, Mater Research Institute, University of Queensland, Woolloongabba, Queensland, Australia [2] School of Medicine, University of Queensland, Brisbane, Queensland, Australia.
Mater Research · AUUniversity of Queensland · AUFibroGen (United States) · USSt Vincents Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many patients with hematological neoplasms fail to mobilize sufficient numbers of hematopoietic stem cells (HSCs) in response to granulocyte colony-stimulating factor (G-CSF) precluding subsequent autologous HSC transplantation. Plerixafor, a specific antagonist of the chemokine receptor CXCR4, can rescue some but not all patients who failed to mobilize with G-CSF alone. These refractory poor mobilizers cannot currently benefit from autologous transplantation. To discover alternative targetable pathways to enhance HSC mobilization, we studied the role of hypoxia-inducible factor-1α (HIF-1α) and the effect of HIF-1α pharmacological stabilization on HSC mobilization in mice. We demonstrate in mice with HSC-specific conditional deletion of the Hif1a gene that the oxygen-labile transcription factor HIF-1α is essential for HSC mobilization in response to G-CSF and Plerixafor. Conversely, pharmacological stabilization of HIF-1α with the 4-prolyl hydroxylase inhibitor FG-4497 synergizes with G-CSF and Plerixafor increasing mobilization of reconstituting HSCs 20-fold compared with G-CSF plus Plerixafor, currently the most potent mobilizing combination used in the clinic.

Indexed as

Hematopoietic Stem Cell MobilizationHematopoietic Stem Cell TransplantationAnimalsAnti-HIV AgentsBenzylaminesBlotting, WesternCell MovementCell ProliferationCells, CulturedCyclamsFlow CytometryGranulocyte Colony-Stimulating FactorHematopoietic Stem CellsHeterocyclic CompoundsHumansHypoxia-Inducible Factor 1, alpha SubunitAnti-HIV AgentsBenzylaminesCyclamsGranulocyte Colony-Stimulating FactorHeterocyclic CompoundsHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitplerixaforProlyl-Hydroxylase InhibitorsProlyl HydroxylasesReceptors, CXCR4RNA, Messenger

Identifiers

PMID25578474
PMCPMC4498452
OpenAlexW2049952763

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.