Evidence map›Paper›PMID 39529098›Full record

ArticleStem cell research & therapy2024

Senolysis potentiates endothelial progenitor cell adhesion to and integration into the brain vasculature.

Tri Duc Lam, István Tóth, Anca Hermenean, Imola Wilhelm, Claudine Kieda, István Krizbai, Attila E Farkas

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Decoding Vascular Senescence: Cellular Insights and Therapeutic Strategies.International journal of biological sciences · 2026
    Review
  4. 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

7 authors.

Tri Duc LamInstitute of Biophysics, HUN-REN Biological Research Centre, Szeged, 6726, Hungary.
István TóthInstitute of Biophysics, HUN-REN Biological Research Centre, Szeged, 6726, Hungary.
Anca HermeneanInstitute of Life Sciences, "Vasile Goldis" Western University of Arad, Arad, 310414, Romania.
Imola WilhelmInstitute of Biophysics, HUN-REN Biological Research Centre, Szeged, 6726, Hungary.
Claudine Kieda *Laboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine-National Research Institute, Warsaw, 04-141, Poland.
István Krizbai *Institute of Biophysics, HUN-REN Biological Research Centre, Szeged, 6726, Hungary. krizbai.istvan@brc.hu.
Attila E Farkas *Institute of Biophysics, HUN-REN Biological Research Centre, Szeged, 6726, Hungary. farkas.attilae@brc.hu.ORCID 0000-0002-9519-5968

Funding

Dr. Rollin D. Hotchkiss Foundation Dr. Rollin D. Hotchkiss FoundationMagyar Tudományos Akadémia NAP2022-I-6Nemzeti Kutatási Fejlesztési és Innovációs Hivatal FK132638Nemzeti Kutatási Fejlesztési és Innovációs Hivatal K135425Nemzeti Kutatási Fejlesztési és Innovációs Hivatal K135475Nemzeti Kutatási Fejlesztési és Innovációs Hivatal TKP2021-EGA-09
6 · The paper itself

Abstract

backgroundOne of the most severe consequences of ageing is cognitive decline, which is associated with dysfunction of the brain microvasculature. Thus, repairing the brain vasculature could result in healthier brain function.

methodsTo better understand the potential beneficial effect of endothelial progenitor cells (EPCs) in vascular repair, we studied the adhesion and integration of EPCs using the early embryonic mouse aorta-gonad-mesonephros - MAgEC 10.5 endothelial cell line. The EPC interaction with brain microvasculature was monitored ex vivo and in vivo using epifluorescence, laser confocal and two-photon microscopy in healthy young and old animals. The effects of senolysis, EPC activation and ischaemia (two-vessel occlusion model) were analysed in BALB/c and FVB/Ant: TgCAG-yfp_sb #27 mice.

resultsMAgEC 10.5 cells rapidly adhered to brain microvasculature and some differentiated into mature endothelial cells (ECs). MAgEC 10.5-derived endothelial cells integrated into microvessels, established tight junctions and co-formed vessel lumens with pre-existing ECs within five days. Adhesion and integration were much weaker in aged mice, but were increased by depleting senescent cells using abt-263 or dasatinib plus quercetin. Furthermore, MAgEC 10.5 cell adhesion to and integration into brain vessels were increased by ischaemia and by pre-activating EPCs with TNFα.

conclusionsCombining progenitor cell therapy with senolytic therapy and the prior activation of EPCs are promising for improving EPC adhesion to and integration into the cerebral vasculature and could help rejuvenate the ageing brain.

Indexed as

BrainCell AdhesionEndothelial Progenitor CellsAnimalsCell DifferentiationCell LineCellular SenescenceDasatinibEndothelial CellsMiceMice, Inbred BALB CMicrovesselsQuercetinSenotherapeuticsTumor Necrosis Factor-alphaDasatinibQuercetinSenotherapeuticsTumor Necrosis Factor-alphaAbt-263AgeingBrainDasatinibEmbryonic endothelial progenitor cellsHypoxiaNavitoclaxQuercetinSenescenceSenolysisVascular regeneration

Identifiers

PMID39529098
PMCPMC11556082

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Registered trials

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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.