Evidence map›Paper›PMID 23807220›Full record

ArticleCell death & disease2013

Human mesenchymal stem cell-replicative senescence and oxidative stress are closely linked to aneuploidy.

J C Estrada, Y Torres, A Benguría, A Dopazo, E Roche, L Carrera-Quintanar, R A Pérez, J A Enríquez, R Torres, J C Ramírez and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
12.3field-weighted citation impact, top 1% 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

116 citing papers in PubMed, 232 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026
    Review
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56 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 1 country.

J C EstradaDepartment of Cardiovascular Development and Repair, Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Melchor Fernández Almagro 3, Madrid, Spain.
Y Torres
A Benguría
A Dopazo
E Roche
L Carrera-Quintanar
R A Pérez
J A Enríquez
R Torres
J C Ramírez
E Samper
A Bernad
Spanish National Centre for Cardiovascular Research · ESUniversitat de Miguel Hernández d'Elx · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In most clinical trials, human mesenchymal stem cells (hMSCs) are expanded in vitro before implantation. The genetic stability of human stem cells is critical for their clinical use. However, the relationship between stem-cell expansion and genetic stability is poorly understood. Here, we demonstrate that within the normal expansion period, hMSC cultures show a high percentage of aneuploid cells that progressively increases until senescence. Despite this accumulation, we show that in a heterogeneous culture the senescence-prone hMSC subpopulation has a lower proliferation potential and a higher incidence of aneuploidy than the non-senescent subpopulation. We further show that senescence is linked to a novel transcriptional signature that includes a set of genes implicated in ploidy control. Overexpression of the telomerase catalytic subunit (human telomerase reverse transcriptase, hTERT) inhibited senescence, markedly reducing the levels of aneuploidy and preventing the dysregulation of ploidy-controlling genes. hMSC-replicative senescence was accompanied by an increase in oxygen consumption rate (OCR) and oxidative stress, but in long-term cultures that overexpress hTERT, these parameters were maintained at basal levels, comparable to unmodified hMSCs at initial passages. We therefore propose that hTERT contributes to genetic stability through its classical telomere maintenance function and also by reducing the levels of oxidative stress, possibly, by controlling mitochondrial physiology. Finally, we propose that aneuploidy is a relevant factor in the induction of senescence and should be assessed in hMSCs before their clinical use.

Indexed as

AneuploidyCellular SenescenceOxidative StressCell Cycle ProteinsCell ProliferationCells, CulturedChemokine CXCL12GelsolinGene ExpressionGene Expression RegulationGenomic InstabilityHumansMesenchymal Stem CellsOxygen ConsumptionReactive Oxygen SpeciesTelomeraseCell Cycle ProteinsChemokine CXCL12CXCL12 protein, humanGelsolinReactive Oxygen SpeciesscinderinTelomerase

Identifiers

PMID23807220
PMCPMC3702285
OpenAlexW2022322309

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.