The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.
Nuclear Erythroid Factor 2-mediated Proteasome Activation Delays Senescence in Human Fibroblasts
Open accessAbstract
Replicative senescence in human fibroblasts is accompanied with alterations of various biological processes, including the impaired function of the proteasome. The proteasome is responsible for the removal of both normal and damaged proteins. Due to its latter function, proteasome is also considered a representative secondary antioxidant cellular mechanism. Nrf2 is a basic transcription factor responsible for the regulation of the cellular antioxidant response that has also been shown to regulate several proteasome subunits in mice. We have established in this study the proteasome-related function of Nrf2 in human fibroblasts undergoing replicative senescence. We demonstrate that Nrf2 has a declined function in senescence, whereas its silencing leads to premature senescence. However, upon its activation by a novel Nrf2 inducer, elevated levels of proteasome activity and content are recorded only in cell lines possessing a functional Nrf2. Moreover, treatment by the Nrf2 inducer results in the enhanced survival of cells following oxidative stress, whereas continuous treatment leads to lifespan extension of human fibroblasts. Importantly the Nrf2-proteasome axis is functional in terminally senescent cultures as these cells retain their responsiveness to the Nrf2 stimuli. In conclusion, these findings open up new directions for future manipulation of the senescence phenotype.
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“silencing Nrf2 gene induces premature senescence”
From Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism (2017) · cites this paper as Kapeta et al., 2010
In the citing paper
“silencing the Nrf2 pathway in human embryonic fibroblasts leads to premature senescence”
From Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism (2017) · cites this paper as Kapeta et al., 2010
In the citing paper
“Studies have found an inverse correlation between aging and Nrf2 expression, both in mouse tissues and in vitro during replicative senescence”
From Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism (2017) · cites this paper as Kapeta et al., 2010
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Transcriptional Regulation by Nrf2
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The Nrf2 regulatory network provides an interface between redox and intermediary metabolism
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NRF2, a Transcription Factor for Stress Response and Beyond
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NRF2 and the Hallmarks of Cancer
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The role of protein clearance mechanisms in organismal ageing and age-related diseases
Vı́lchez, D., Sáez, I., & Dillin, A. G. (2014) · Nature Communications · doi:10.1038/ncomms6659 · Cited by 710
Metadata
- Authors
- Kapeta, S., Chondrogianni, N., & Gonos, E. S.
- Affiliations
- National Hellenic Research Foundation (GR)
- Corresponding author
- Chondrogianni, Niki
- Gonos, Efstathios S.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2010-03
- Volume
- 285
- Issue
- 11
- Pages
- 8171-8184
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC2832969
- OpenAlex
- W2075571292
- Cited by
- 234
- References
- 59
- Citations by year
- 2026: 11 · 2025: 12 · 2024: 20 · 2023: 14 · 2022: 19 · 2021: 13 · 2020: 23 · 2019: 16 · 2018: 15 · 2017: 20 · 2016: 15 · 2015: 8 · 2014: 16 · 2013: 7 · 2012: 13
- FWCI
- 4.17
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- National Hellenic Research Foundation Helios Repository (National Hellenic Research Foundation) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- Nrf2, proteasome, replicative senescence, human fibroblasts, premature senescence, Nrf2 inducers, oxidative stress, lifespan extension, protein degradation, senescence reversal
- MeSH terms
- Cell Division, Cell Line, Enzyme Activation, Fibroblasts, Glycyrrhetinic Acid, Humans, Luciferases, Down-Regulation, Cellular Senescence, Reactive Oxygen Species, Oxidative Stress, RNA Interference, Proteasome Endopeptidase Complex, NF-E2-Related Factor 2
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