Evidence mapPaperPMID 41226300Full record

ArticleInternational journal of molecular sciences2025

Urolithin A Alleviates Doxorubicin-Induced Senescence in Mesenchymal Stem Cells.

Alexander Kalinin, Ekaterina Zubkova, Mikhail Menshikov, Yelena Parfyonova

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Alexander KalininNational Medical Research Centre of Cardiology Named After Academician E.I. Chazov, Moscow 121552, Russia.ORCID 0000-0002-9668-3832
Ekaterina ZubkovaNational Medical Research Centre of Cardiology Named After Academician E.I. Chazov, Moscow 121552, Russia.ORCID 0000-0002-0512-3670
Mikhail MenshikovNational Medical Research Centre of Cardiology Named After Academician E.I. Chazov, Moscow 121552, Russia.
Yelena ParfyonovaNational Medical Research Centre of Cardiology Named After Academician E.I. Chazov, Moscow 121552, Russia.

Funding

Russian Science Foundation 23-15-00539
6 · The paper itself

Abstract

The accumulation of senescent cells, characterized by a pro-inflammatory secretory phenotype (SASP), metabolic dysfunction, and irreversible cell cycle arrest, is a driving force behind numerous age-related pathologies and directly undermines the therapeutic potential of mesenchymal stem cells (MSCs). In this study, we explore the senotherapeutic potential of urolithin A, a renowned antioxidant compound, in human adipose-derived MSCs (AD-hMSCs). Our findings reveal that urolithin A is non-cytotoxic to senescent AD-hMSCs and significantly suppresses the SASP by reducing the secretion of key pro-inflammatory mediators, including MCP1, PAI2, and IL1B. In addition, it was demonstrated that urolithin A was capable of reversing the decline in H3K9me3 levels induced by Doxorubicin treatment, restoring them to levels observed in untreated cells. The results of this study suggest that urolithin A functions as a senomorphic agent, capable of modulating cellular senescence. Moreover, its combination with senolytic therapies has the potential to yield novel and effective treatment strategies for regenerative medicine.

Indexed as

Cellular SenescenceCoumarinsDoxorubicinMesenchymal Stem CellsCells, CulturedHumans3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-oneCoumarinsDoxorubicinagingautophagycellular senescencedoxorubicinmesenchymal stem cellssenotherapeutics

Identifiers

PMID41226300
PMCPMC12608000

What Socratic 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 Socratic graph.