Evidence map›Paper›PMID 29022209›Full record

ArticleInternational journal of hematology2018

Therapeutic doses of doxorubicin induce premature senescence of human mesenchymal stem cells derived from menstrual blood, bone marrow and adipose tissue.

Irina Kozhukharova, Victoria Zemelko, Zoya Kovaleva, Larisa Alekseenko, Olga Lyublinskaya, Nikolay Nikolsky

Abstract read
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In one paragraph

Article in International journal of hematology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Doxorubicin-Induced Cytotoxicity in Adipose-Derived Stem Cells Is Associated With Altered SAPK/JNK Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

6 authors at 1 institution in 1 country.

Irina KozhukharovaDepartment of Intracellular Signaling and Transport, Institute of Cytology Russian Academy of Sciences, Tikhoretskiy Prospect 4, Saint-Petersburg, 194064, Russia. kojuxarova@mail.ru.ORCID http://orcid.org/0000-0002-7616-9510
Victoria ZemelkoDepartment of Intracellular Signaling and Transport, Institute of Cytology Russian Academy of Sciences, Tikhoretskiy Prospect 4, Saint-Petersburg, 194064, Russia.
Zoya KovalevaDepartment of Intracellular Signaling and Transport, Institute of Cytology Russian Academy of Sciences, Tikhoretskiy Prospect 4, Saint-Petersburg, 194064, Russia.
Larisa AlekseenkoDepartment of Intracellular Signaling and Transport, Institute of Cytology Russian Academy of Sciences, Tikhoretskiy Prospect 4, Saint-Petersburg, 194064, Russia.
Olga LyublinskayaDepartment of Intracellular Signaling and Transport, Institute of Cytology Russian Academy of Sciences, Tikhoretskiy Prospect 4, Saint-Petersburg, 194064, Russia.
Nikolay NikolskyDepartment of Intracellular Signaling and Transport, Institute of Cytology Russian Academy of Sciences, Tikhoretskiy Prospect 4, Saint-Petersburg, 194064, Russia.
Institute of Cytology · RU

Funding

The work was supported by the Russian Science Foundation . project 14-50-00068
6 · The paper itself

Abstract

Doxorubicin (Dox) is an effective anticancer drug with known activity against a wide spectrum of malignancies, hematologic malignancies in particular. Despite extensive clinical use, the mechanisms of its side effects and negative action on normal cells remain under study. The aim of this study was to investigate the effect of Dox on cultured human mesenchymal stem cells (MSCs) derived from menstrual blood (eMSCs), bone marrow (BMSCs) and adipose tissue (AMSCs). Dox treatment in high doses decreased the survival of MSCs in a dose-dependent manner. Clinically relevant low doses of Dox induced premature senescence of eMSCs, BMSCs and AMSCs, but did not kill the cells. Dox caused cell cycle arrest and formation of γ-H2AX foci, and increased the number of SA-β-gal-positive cells. BMSCs entered premature senescence earlier than other MSCs. It has been reported that neural-like cells differentiated from MSCs of various origins are more sensitive to Dox than their parent cells. Dox-treated differentiated MSCs exhibited lower viability and earlier generation of γ-H2AX foci. Dox administration inhibited secretory activity in neural-like cells. These findings suggest that a clinically relevant Dox dose damages cultured MSCs, inducing their premature senescence. MSCs are more resistant to this damage than differentiated cells.

Indexed as

MenstruationAdipose TissueAntineoplastic AgentsBlood CellsBone Marrow CellsCell Cycle CheckpointsCell DifferentiationCells, CulturedCellular SenescenceDose-Response Relationship, DrugDoxorubicinHistonesHumansMesenchymal Stem CellsAntineoplastic AgentsDoxorubicinH2AX protein, humanHistonesDoxorubicinMesenchymal stem cellsStress-induced premature senescenceγ-H2AX foci

Identifiers

PMID29022209
OpenAlexW2761734802

What OpenQuestion holds

Textmetadata
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.