Evidence map›Paper›PMID 27498709›Full record

ArticleInternational journal of molecular medicine2016

Epigallocatechin-3-gallate prevents oxidative stress-induced cellular senescence in human mesenchymal stem cells via Nrf2.

Joo-Hyun Shin, Hyo-Jin Jeon, Jihye Park, Mi-Sook Chang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 81 citations in OpenAlex.

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  16. Frontiers in veterinary science · 2025
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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

4 authors at 1 institution in 1 country.

Joo-Hyun ShinLaboratory of Stem Cell and Neurobiology, Department of Oral Anatomy, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 03080, Republic of Korea.
Hyo-Jin JeonLaboratory of Stem Cell and Neurobiology, Department of Oral Anatomy, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 03080, Republic of Korea.
Jihye ParkLaboratory of Stem Cell and Neurobiology, Department of Oral Anatomy, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 03080, Republic of Korea.
Mi-Sook ChangLaboratory of Stem Cell and Neurobiology, Department of Oral Anatomy, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 03080, Republic of Korea.
Seoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human mesenchymal stem cells (hMSCs) have great therapeutic potential due to their high plasticity, immune privileged status and ease of preparation, as well as a lack of ethical barriers to their use. However, their ultimate usefulness is limited by cellular senescence occurring secondary to increased cellular levels of reactive oxygen species (ROS) during their propagation in culture. The underlying molecular mechanisms responsible for this process in hMSCs remain unclear. An antioxidant polyphenol epigallocatechin-3-gallate (EGCG) found in green tea, is known to activate nuclear factor-erythroid 2-related factor 2 (Nrf2), a master transcriptional regulator of antioxidant genes. Herein, we examined the EGCG-mediated antioxidant mechanism in hMSCs exposed to ROS which involves Nrf2 activation. The H2O2-exposed hMSCs showed cellular senescence with significantly increased protein levels of acetyl-p53 and p21 in comparison with the untreated hMSCs, and these effects were prevented by pre-treatment with EGCG. By contrast, in Nrf2-knockdown hMSCs, EGCG lost its antioxidant effect, exhibiting high levels of acetyl-p53 and p21 following EGCG pre-treatment and H2O2 exposure. This indicates that Nrf2 and p53/p21 may be involved in the anti‑senescent effect of EGCG in hMSCs. Taken together, these findings indicate the important role of EGCG in preventing oxidative stress-induced cellular senescence in hMSCs through Nrf2 activation, which has applications for the massive production of more suitable hMSCs for cell-based therapy.

Indexed as

AcetylationAdultCatechinCell NucleusCellular SenescenceCyclin-Dependent Kinase Inhibitor p21HumansHydrogen PeroxideMesenchymal Stem CellsModels, BiologicalNF-E2-Related Factor 2Oxidative StressProtein TransportTumor Suppressor Protein p53CatechinCyclin-Dependent Kinase Inhibitor p21epigallocatechin gallateHydrogen PeroxideNF-E2-Related Factor 2Tumor Suppressor Protein p53

Identifiers

PMID27498709
PMCPMC5029951
OpenAlexW2479397168

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.