Evidence map›Paper›PMID 31983656›Full record

ArticleStem cell reports2020

Senescence-Associated Metabolomic Phenotype in Primary and iPSC-Derived Mesenchymal Stromal Cells.

Eduardo Fernandez-Rebollo, Julia Franzen, Roman Goetzke, Jonathan Hollmann, Alina Ostrowska, Matteo Oliverio, Torsten Sieben, Björn Rath, Jan-Wilhelm Kornfeld, Wolfgang Wagner

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 90 citations in OpenAlex.

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  7. RNA sequencing identifiesCytotechnology · 2025
    Article
  8. Article
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  12. Genetic and Epigenetic Interactions Involved in Senescence of Stem Cells.International journal of molecular sciences · 2024
    Review
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  15. Article
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  19. Article
  20. Biomarkers of aging.Science China. Life sciences · 2023
    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

10 authors at 4 institutions in 2 countries.

Eduardo Fernandez-RebolloHelmholtz-Institute for Biomedical Engineering, Stem Cell Biology and Cellular Engineering, RWTH Aachen University Medical School, Aachen 52074, Germany; Institute for Biomedical Technology - Cell Biology, RWTH Aachen University Medical School, Aachen 52074, Germany; University of Southern Denmark, Functional Genomics and Metabolism Unit, Department for Biochemistry and Molecular Biology, Campusvej 55, Odense 5230, Denmark. Electronic address: ef-r@bmb.sdu.dk.
Julia FranzenHelmholtz-Institute for Biomedical Engineering, Stem Cell Biology and Cellular Engineering, RWTH Aachen University Medical School, Aachen 52074, Germany; Institute for Biomedical Technology - Cell Biology, RWTH Aachen University Medical School, Aachen 52074, Germany.
Roman GoetzkeHelmholtz-Institute for Biomedical Engineering, Stem Cell Biology and Cellular Engineering, RWTH Aachen University Medical School, Aachen 52074, Germany; Institute for Biomedical Technology - Cell Biology, RWTH Aachen University Medical School, Aachen 52074, Germany.
Jonathan HollmannHelmholtz-Institute for Biomedical Engineering, Stem Cell Biology and Cellular Engineering, RWTH Aachen University Medical School, Aachen 52074, Germany; Institute for Biomedical Technology - Cell Biology, RWTH Aachen University Medical School, Aachen 52074, Germany.
Alina OstrowskaHelmholtz-Institute for Biomedical Engineering, Stem Cell Biology and Cellular Engineering, RWTH Aachen University Medical School, Aachen 52074, Germany; Institute for Biomedical Technology - Cell Biology, RWTH Aachen University Medical School, Aachen 52074, Germany.
Matteo OliverioMax Planck Institute for Metabolism Research (MPI-MR), Noncoding RNAs and Energy Homeostasis, Gleueler Strasse 50, Cologne 50931, Germany; Cologne Cluster of Excellence: Cellular Stress Responses in Aging-Associated Diseases (CECAD), Cologne 50931, Germany.
Torsten SiebenHelmholtz-Institute for Biomedical Engineering, Stem Cell Biology and Cellular Engineering, RWTH Aachen University Medical School, Aachen 52074, Germany; Institute for Biomedical Technology - Cell Biology, RWTH Aachen University Medical School, Aachen 52074, Germany.
Björn RathDepartment for Orthopedics, RWTH Aachen University Medical School, Aachen 52074, Germany.
Jan-Wilhelm KornfeldMax Planck Institute for Metabolism Research (MPI-MR), Noncoding RNAs and Energy Homeostasis, Gleueler Strasse 50, Cologne 50931, Germany; Cologne Cluster of Excellence: Cellular Stress Responses in Aging-Associated Diseases (CECAD), Cologne 50931, Germany; University of Southern Denmark, Functional Genomics and Metabolism Unit, Department for Biochemistry and Molecular Biology, Campusvej 55, Odense 5230, Denmark.
Wolfgang WagnerHelmholtz-Institute for Biomedical Engineering, Stem Cell Biology and Cellular Engineering, RWTH Aachen University Medical School, Aachen 52074, Germany; Institute for Biomedical Technology - Cell Biology, RWTH Aachen University Medical School, Aachen 52074, Germany. Electronic address: wwagner@ukaachen.de.
RWTH Aachen University · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEMax Planck Institute for Metabolism Research · DEUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long-term culture of primary cells is characterized by functional and secretory changes, which ultimately result in replicative senescence. It is largely unclear how the metabolome of cells changes during replicative senescence and if such changes are consistent across different cell types. We have directly compared culture expansion of primary mesenchymal stromal cells (MSCs) and induced pluripotent stem cell-derived MSCs (iMSCs) until they reached growth arrest. Both cell types acquired similar changes in morphology, in vitro differentiation potential, senescence-associated β-galactosidase, and DNA methylation. Furthermore, MSCs and iMSCs revealed overlapping gene expression changes, particularly in functional categories related to metabolic processes. We subsequently compared the metabolomes of MSCs and iMSCs and observed overlapping senescence-associated changes in both cell types, including downregulation of nicotinamide ribonucleotide and upregulation of orotic acid. Taken together, replicative senescence is associated with a highly reproducible senescence-associated metabolomics phenotype, which may be used to monitor the state of cellular aging.

Indexed as

Cellular SenescenceMetabolomicsAgedCells, CulturedEnergy MetabolismGene Expression ProfilingGene Expression RegulationHumansInduced Pluripotent Stem CellsMesenchymal Stem CellsMetabolic Networks and PathwaysMetabolomeMiddle AgedPhenotypeDNA methylationinduced pluripotent stem cellsmesenchymal stromal cellsmetabolomicsreplicative senescencetranscriptomics

Identifiers

PMID31983656
PMCPMC7013233
OpenAlexW3001481865

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.