ArticleBMB reports2017
Peroxiredoxin I participates in the protection of reactive oxygen species-mediated cellular senescence.
Article in BMB reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Redox metabolism in cell senescence: focusing on contributions from the metabolomic field.Frontiers in molecular biosciences · 2025Review
- Conditional knockout mouse model reveals a critical role of peroxiredoxin 1 in oral leukoplakia carcinogenesis.Heliyon · 2024Article
- Exercise, healthy ageing, and the potential role of small extracellular vesicles.The Journal of physiology · 2023Article
- Peroxiredoxin, Senescence, and Cancer.Cells · 2022Review
- Peroxiredoxin1 Knockdown Inhibits Oral Carcinogenesis via Inducing Cell Senescence Dependent on Mitophagy.OncoTargets and therapy · 2021Article
- Single-cell RNA sequencing of murine islets shows high cellular complexity at all stages of autoimmune diabetes.The Journal of experimental medicine · 2020Article
- Knockout Mouse Models for Peroxiredoxins.Antioxidants (Basel, Switzerland) · 2020Review
- Highly Purified Human Extracellular Vesicles Produced by Stem Cells Alleviate Aging Cellular Phenotypes of Senescent Human Cells.Stem cells (Dayton, Ohio) · 2019Article
- Real-time PCR quantification of spliced X-box binding protein 1 (XBP1) using a universal primer method.PloS one · 2019Article
- Targeting peroxiredoxin 1 impairs growth of breast cancer cells and potently sensitises these cells to prooxidant agents.British journal of cancer · 2018Article
- Potential Applications of Non-thermal Plasma in Animal Husbandry to Improve Infrastructure.In vivo (Athens, Greece)Review
- Protective Role of Peroxiredoxin I in Heat-KilledIn vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peroxiredoxin I (Prx I) plays an important role as a reactive oxygen species (ROS) scavenger in protecting and maintaining cellular homeostasis; however, the underlying mechanisms are not well understood. Here, we identified a critical role of Prx I in protecting cells against ROS-mediated cellular senescence by suppression of p16INK4a expression. Compared to wild-type mouse embryonic fibroblasts (WT-MEFs), Prx I-/- MEFs exhibited senescence-associated phenotypes. Moreover, the aged Prx I-/- mice showed an increased number of cells with senescence associated-β-galactosidase (SA-β-gal) activity in a variety of tissues. Increased ROS levels and SA-β-gal activity, and reduction of chemical antioxidant further in Prx I-/- MEF supported an essential role of Prx I peroxidase activity in cellular senescence that is mediated by oxidative stress. The up-regulation of p16INK4a expression in Prx I-/- and suppression by overexpression of Prx I indicate that Prx I possibly modulate cellular senescence through ROS/p16INK4a pathway. [BMB Reports 2017; 50(10): 528-533].
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