Evidence map›Paper›PMID 40298797›Full record

ArticleAntioxidants (Basel, Switzerland)2025

Replicative Senescence in Mesenchymal Stem Cells: An In Vitro Study on Mitochondrial Dynamics and Metabolic Alterations.

Beatrice Casorati, Isabella Zafferri, Sara Castiglioni, Jeanette A Maier

Abstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Review
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  3. Article
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  5. Article
  6. Article
  7. Review
  8. Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026
    Review
  9. Article
  10. Review
  11. 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

4 authors.

Beatrice CasoratiDepartment of Biomedical and Clinical Sciences, Università di Milano, 20157 Milano, Italy.ORCID 0009-0000-5644-7897
Isabella ZafferriDepartment of Biomedical and Clinical Sciences, Università di Milano, 20157 Milano, Italy.ORCID 0009-0005-2989-9114
Sara CastiglioniDepartment of Biomedical and Clinical Sciences, Università di Milano, 20157 Milano, Italy.ORCID 0000-0002-8785-9891
Jeanette A MaierDepartment of Biomedical and Clinical Sciences, Università di Milano, 20157 Milano, Italy.ORCID 0000-0002-6326-9221

Funding

European Union-Next Generation EU 2022KM2MBT_003
6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) are multipotent progenitors capable of self-renewal and differentiation into various cell lineages, making them essential for tissue repair and regenerative medicine. However, their regenerative potential is constrained by replicative senescence, an irreversible growth arrest that occurs after a finite number of cell divisions. In this study, we serially passaged human bone marrow-derived MSCs (bMSCs) and compared young, pre-senescent, and senescent cells. The onset of senescence was accompanied by progressive alterations in mitochondrial dynamics, leading to a decline in mitochondrial membrane potential, and increased reactive oxygen species (ROS) production, alongside a diminished cellular antioxidant capacity. These mitochondrial defects play a role in metabolic reprogramming in senescent bMSCs. Our findings underscore the intricate interplay between ROS, mitochondrial dysfunction, and replicative senescence, offering valuable insights to guide the development of therapeutic strategies for preserving MSC functionality in aging and MSC-based therapies.

Indexed as

mesenchymal stem cellsmitochondriareplicative senescenceROS

Identifiers

PMID40298797
PMCPMC12024194

What OpenQuestion holds

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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.