ArticleOxidative medicine and cellular longevity2012
Preventive effects of epigallocatechin-3-O-gallate against replicative senescence associated with p53 acetylation in human dermal fibroblasts.
Article in Oxidative medicine and cellular longevity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Pooled it
- The Antiaging Potential of Dietary Plant-Based Polyphenols: A Review on Their Role in Cellular Senescence Modulation.Nutrients · 2025Review
- Green Tea Mitigates the Hallmarks of Aging and Age-Related Multisystem Deterioration.Aging and disease · 2025Review
- Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential.Molecules (Basel, Switzerland) · 2025Review
- The Potential of Polyphenols in Modulating the Cellular Senescence Process: Implications and Mechanism of Action.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Decoding senescence of aging single cells at the nexus of biomaterials, microfluidics, and spatial omics.npj aging · 2024Review
- Revolutionizing Diabetic Foot Ulcer Care: The Senotherapeutic Approach.Aging and disease · 2024Review
- (-)-Epigallocatechin-3-gallate induced apoptosis by dissociation of c-FLIP/Ku70 complex in gastric cancer cells.Journal of cellular and molecular medicine · 2023Article
- Co-inhibition of ATM and ROCK synergistically improves cell proliferation in replicative senescence by activating FOXM1 and E2F1.Communications biology · 2022Article
- An Insight into Aging, Senescence, and Their Impacts on Wound Healing.Advances in geriatric medicine and research · 2021Article
- Preclinical Pharmacological Activities of Epigallocatechin-3-gallate in Signaling Pathways: An Update on Cancer.Molecules (Basel, Switzerland) · 2020Review
- Effect of Antioxidants on the Fibroblast Replicative LifespanOxidative medicine and cellular longevity · 2020Review
- An Appraisal on the Value of Using Nutraceutical Based Senolytics and Senostatics in Aging.Frontiers in cell and developmental biology · 2020Review
- Inactivation of TFEB and NF-Acta pharmaceutica Sinica. B · 2019Article
- Polyphenol Polymerization by an Alternative Oxidative Microbial Enzyme and Characterization of the Biological Activity of Oligomers.BioMed research international · 2018Article
- Epigallocatechin-3-gallate prevents oxidative stress-induced cellular senescence in human mesenchymal stem cells via Nrf2.International journal of molecular medicine · 2016Article
- Histone and Non-Histone Targets of Dietary Deacetylase Inhibitors.Current topics in medicinal chemistry · 2016Review
- New nucleophilic mechanisms of ros-dependent epigenetic modifications: comparison of aging and cancer.Aging and disease · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Considering the various pharmacological activities of epigallocatechin-3-O-gallate (EGCG) including anticancer, and anti-inflammatory, antidiabetic, and so forth, relatively less attention has been paid to the antiaging effect of EGCG on primary cells. In this study, the preventive effects of EGCG against serial passage-induced senescence were investigated in primary cells including rat vascular smooth muscle cells (RVSMCs), human dermal fibroblasts (HDFs), and human articular chondrocytes (HACs). The involvement of Sirt1 and acetylated p53 was examined as an underlying mechanism for the senescence preventive activity of EGCG in HDFs. All cells were employed with the initial passage number (PN) between 3 and 7. For inducing senescence, the cells were serially passaged at the predetermined times and intervals in the absence or presence of EGCG (50 or 100 μM). Serial passage-induced senescence in RVSMCs and HACs was able to be significantly prevented at 50 μM EGCG, while in HDFs, 100 μM EGCG could significantly prevent senescence and recover their cell cycle progression close to the normal level. Furthermore, EGCG was found to prevent serial passage- and H(2)O(2)-induced senescence in HDFs by suppressing p53 acetylation, but the Sirt1 activity was unaffected. In addition, proliferating HDFs showed similar cellular uptake of FITC-conjugated EGCG into the cytoplasm with their senescent counterparts but different nuclear translocation of it from them, which would partly account for the differential responses to EGCG in proliferating versus senescent cells. Taking these results into consideration, it is suggested that EGCG may be exploited to craft strategies for the development of an antiaging or age-delaying agent.
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Registered trials
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.