Evidence map›Paper›PMID 23315165›Full record

ArticleBlood2013

The function of hematopoietic stem cells is altered by both genetic and inflammatory factors in lupus mice.

Haitao Niu, Guoqiang Fang, Yiting Tang, Luokun Xie, Huan Yang, Laurence Morel, Betty Diamond, Yong-Rui Zou

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Dysregulated Bone Marrow Contributes to Glomerular Injury through Soluble Factors.Journal of the American Society of Nephrology : JASN · 2026
    Article
  2. Article
  3. Stem cell-based therapy for systemic lupus erythematous.Journal of translational autoimmunity · 2024
    Review
  4. Article
  5. Article
  6. Stem Cell Therapy in Lupus.Rheumatology and immunology research · 2022
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
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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 1 country.

Haitao NiuThe Center for Autoimmune and Musculoskeletal Disease, The Feinstein Institute for Medical Research, North Shore-LIJ Health System, Manhasset, NY, USA.
Guoqiang Fang
Yiting Tang
Luokun Xie
Huan Yang
Laurence Morel
Betty Diamond
Yong-Rui Zou
Autoimmune Technologies (United States) · USFeinstein Institute for Medical Research · USNorthwell Health · USUniversity of Florida · US

Funding

Genetic dissection of Sle2 contribution to SLE pathogenesisR01AI068965 · NIAID · UNIVERSITY OF FLORIDA · PI MOREL, LAURENCE · 2006 to 2010
$1.7M
NIAID NIH HHS R01 AI068965NIAID NIH HHS R01AI068965
6 · The paper itself

Abstract

Hematopoietic stem cells (HSCs) are protected in a metabolically dormant state within the bone marrow stem cell niche. Inflammation has been shown to disrupt HSC dormancy and cause multiple functional changes. Here, we investigated whether HSC functions were altered in systemic lupus erythematosus (SLE)-prone mice and whether this contributed to clinical manifestations of SLE. We found that HSCs were significantly expanded in lupus mice. The increase in HSC cellularity was caused by both genetic lupus risk factors and inflammatory cytokines in lupus mice. In addition, the inflammatory conditions of lupus led to HSC mobilization and lineage-biased hematopoiesis. Strikingly, these functionally altered HSCs possessed robust self-renewal capacity and exhibited repopulating advantages over wild-type HSCs. A single-nucleotide polymorphism in the cdkn2c gene encoding p18(INK4c) within a SLE susceptibility locus was found to account for reduced p18(INK4c) expression and the increase in HSC self-renewal capacity in lupus mice. Lupus HSCs with enhanced self-renewal capacity and resistance to stress may compete out transplanted healthy HSCs, thereby leading to relapses after HSC transplantation.

Indexed as

AnimalsCell ProliferationCell SurvivalCyclin-Dependent Kinase Inhibitor p18Cyclin-Dependent Kinase Inhibitor p21Gene Expression RegulationHematopoietic Stem CellsInflammation MediatorsLupus Erythematosus, SystemicMiceMice, CongenicMice, Inbred C57BLMyelopoiesisSignal TransductionCdkn2c protein, mouseCyclin-Dependent Kinase Inhibitor p18Cyclin-Dependent Kinase Inhibitor p21Inflammation Mediators

Identifiers

PMID23315165
PMCPMC3596961
OpenAlexW2012514252

What OpenQuestion holds

Textmetadata
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.