Evidence map›Paper›PMID 33805981›Full record

ArticleInternational journal of molecular sciences2021

Therapeutic Potential for Regulation of the Nuclear Factor Kappa-B Transcription Factor p65 to Prevent Cellular Senescence and Activation of Pro-Inflammatory in Mesenchymal Stem Cells.

Rocío Mato-Basalo, Miriam Morente-López, Onno J Arntz, Fons A J van de Loo, Juan Fafián-Labora, María C Arufe

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-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

31 citing papers in PubMed, 38 citations in OpenAlex.

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  11. A CommonOxidative medicine and cellular longevity · 2025
    Article
  12. Immune aging and infectious diseases.Chinese medical journal · 2024
    Review
  13. Article
  14. Article
  15. Cellular Senescence: A Troy Horse in Pulmonary Fibrosis.International journal of molecular sciences · 2023
    Review
  16. Review
  17. Article
  18. Article
  19. Article
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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 2 institutions in 3 countries.

Rocío Mato-BasaloGrupo de Terapia Celular y Medicina Regenerativa, Departamento de Fisioterapia, Ciencias Biomédicas y Medicina, Universdidade da Coruña, 15006 A Coruña, Spain.ORCID 0000-0001-6321-7731
Miriam Morente-LópezGrupo de Terapia Celular y Medicina Regenerativa, Departamento de Fisioterapia, Ciencias Biomédicas y Medicina, Universdidade da Coruña, 15006 A Coruña, Spain.
Onno J ArntzExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525 GA Nijmegen, The Netherlands.
Fons A J van de LooExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525 GA Nijmegen, The Netherlands.
Juan Fafián-LaboraGrupo de Terapia Celular y Medicina Regenerativa, Departamento de Fisioterapia, Ciencias Biomédicas y Medicina, Universdidade da Coruña, 15006 A Coruña, Spain.
María C ArufeGrupo de Terapia Celular y Medicina Regenerativa, Departamento de Fisioterapia, Ciencias Biomédicas y Medicina, Universdidade da Coruña, 15006 A Coruña, Spain.ORCID 0000-0003-3725-0743
Universidade da Coruña · ESRadboud University Nijmegen · NL

Funding

Instituto de Salud Carlos III PI20/00497Xunta de Galicia ED481B 2017/117
6 · The paper itself

Abstract

Mesenchymal stem cells have an important potential in the treatment of age-related diseases. In the last years, small extracellular vesicles derived from these stem cells have been proposed as cell-free therapies. Cellular senescence and proinflammatory activation are involved in the loss of therapeutic capacity and in the phenomenon called inflamm-aging. The regulators of these two biological processes in mesenchymal stem cells are not well-known. In this study, we found that p65 is activated during cellular senescence and inflammatory activation in human umbilical cord-derived mesenchymal stem cell. To demonstrate the central role of p65 in these two processes, we used small-molecular inhibitors of p65, such as JSH-23, MG-132 and curcumin. We found that the inhibition of p65 prevents the cellular senescence phenotype in human umbilical cord-derived mesenchymal stem cells. Besides, p65 inhibition produced the inactivation of proinflammatory molecules as components of a senescence-associated secretory phenotype (SASP) (interleukin-6 and interleukin-8 (IL-6 and IL-8)). Additionally, we found that the inhibition of p65 prevents the transmission of paracrine senescence between mesenchymal stem cells and the proinflammatory message through small extracellular vesicles. Our work highlights the important role of p65 and its inhibition to restore the loss of functionality of small extracellular vesicles from senescent mesenchymal stem cells and their inflamm-aging signature.

Indexed as

AdolescentAdultCell ProliferationCells, CulturedCellular SenescenceCurcuminDNA DamageFemaleHumansInflammationLeupeptinsMesenchymal Stem CellsNanoparticlesParacrine CommunicationPhenotypePhenylenediamines4-methyl-N1-(3-phenylpropyl)benzene-1,2-diaminebenzyloxycarbonylleucyl-leucyl-leucine aldehydeCurcuminLeupeptinsPhenylenediaminesRELA protein, humanTranscription Factor RelAcellular senescenceinflamm-agingmesenchymal stem cellsSASPsEV

Identifiers

PMID33805981
PMCPMC8038109
OpenAlexW3138147475

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.