Evidence map›Paper›PMID 23615056›Full record

ReviewCurrent opinion in hematology2013

Cdc42 and aging of hematopoietic stem cells.

Hartmut Geiger, Yi Zheng

Abstract readReview
In one paragraph

Review in Current opinion in hematology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. The Regenerative Power of Stem Cells: Treating Bleomycin-Induced Lung Fibrosis.Stem cells and cloning : advances and applications · 2023
    Review
  4. Article
  5. Review
  6. Review
  7. Genes and Longevity of Lifespan.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Article
  10. Frontiers in cell and developmental biology · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Changing mutational and adaptive landscapes and the genesis of cancer.Biochimica et biophysica acta. Reviews on cancer · 2017
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

2 authors at 2 institutions in 2 countries.

Hartmut GeigerDepartment of Dermatology and Allergic Diseases, University of Ulm, Ulm, Germany. hartmut.geiger@uni-ulm.de
Yi Zheng
Universität Ulm · DEUniversity of Cincinnati · US

Funding

Lineage Determination and Tissue HomeOstasis in the aged Hematopoietic SystemR01AG040118 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI GEIGER, HARTMUT, ZHENG, YI · 2011 to 2015
$1.7M
Genetic Reg. of Hematopoietic Stem Cell MobilizationR01HL076604 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI GEIGER, HARTMUT · 2004 to 2007
$1.2M
Young Stem Cell Potential in Aged MiceR21DK077762 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI GEIGER, HARTMUT · 2008 to 2009
$413k
NHLBI NIH HHS HL076604NHLBI NIH HHS R01 HL076604NIA NIH HHS AG040118NIA NIH HHS R01 AG040118NIDDK NIH HHS DK077762NIDDK NIH HHS R21 DK077762
6 · The paper itself

Abstract

purpose of reviewHematopoietic stem cells (HSCs) continuously provide mature blood cells during the lifespan of a mammal. The functional decline in hematopoiesis in the elderly, which involves a progressive reduction in the immune response and an increased incidence of myeloid malignancy, is partly linked to HSC aging. Molecular mechanisms of HSC aging remain unclear, hindering rational approaches to slow or reverse the decline of HSC function with age. Identifying conditions under which aged HSCs become equivalent to young stem cells might result in treatments for age-associated imbalances in lymphopoiesis and myelopoiesis and in blood regeneration. RECENT

findingsAging of HSCs has been for a long time thought to be an irreversible process imprinted in stem cells due to the intrinsic nature of HSC aging. Mouse model studies have found that aging is associated with elevated activity of the Rho GTPase Cdc42 in HSCs that is causative for loss of polarity, altered epigenetic modifications and functional deficits of aged HSCs. The work suggests that inhibition of Cdc42 activity in aged HSCs may reverse a number of phenotypes associated with HSC aging. SUMMARY: Maintaining the regenerative capacity of organs or organ systems may be a useful way to ensure healthy aging. A defined set of features phenotypically separate young from aged HSCs. Aging of HSCs has been thought to be irreversible. Recent findings support the hypothesis that functional decline of aged HSCs may be reversible by pharmacological intervention of age altered signaling pathways and epigenetic modifications.

Indexed as

AgingAnimalscdc42 GTP-Binding ProteinCellular SenescenceHematopoiesisHematopoietic Stem CellsHumansMiceModels, AnimalSignal Transductioncdc42 GTP-Binding Protein

Identifiers

PMID23615056
PMCPMC4057184
OpenAlexW1995084758

What OpenQuestion holds

Textmetadata
LicenceTDM
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.