ArticleAging2014
Interaction between ROS dependent DNA damage, mitochondria and p38 MAPK underlies senescence of human adult stem cells.
Article in Aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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.
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.
Who cites it
107 citing papers in PubMed, 202 citations in OpenAlex.
- Extracellular ATP drives tryptophan metabolism and aryl hydrocarbon receptor activation to promote cellular senescence.The Journal of biological chemistry · 2026Article
- Endometrial senescence: inevitability and conditional occurrence in female fertility.Reproduction & fertility · 2026Review
- Synergistic protective and regenerative effects of hyaluronic acid and polynucleotides against UVA-induced oxidative stress in dermal fibroblasts.Scientific reports · 2026Article
- Inflammatory bone loss and signaling pathways in periodontitis: mechanistic insights and emerging therapeutic strategies.Bone research · 2026Review
- A narrative review of therapy-induced senescence in cancer: mechanisms, immune interplay, and therapeutic opportunities.Journal of the Egyptian National Cancer Institute · 2025Review
- Targeting tumor metabolic flexibility enhances radiotherapeutic efficacy via mitochondrial complex I Inhibition in an intracranial S180 sarcoma mouse model.Scientific reports · 2025Article
- Endometrial Microbiome and Reproductive Receptivity: Diverse Perspectives.International journal of molecular sciences · 2025Review
- Targeting PON2 with Vutiglabridin Restores Mitochondrial Integrity and Attenuates Oxidative Stress-Induced Senescence.Antioxidants (Basel, Switzerland) · 2025Article
- Mitochondrial Dynamics in Aging Heart.Biomedicines · 2025Review
- Oxidative Stress-Driven Cellular Senescence: Mechanistic Crosstalk and Therapeutic Horizons.Antioxidants (Basel, Switzerland) · 2025Review
- p38 mitogen-activated protein kinase drives senescence in CD4Immunity & ageing : I & A · 2025Article
- Dynamic Interplay Between Autophagy and Oxidative Stress in Stem Cells: Implications for Regenerative Medicine.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- Preventing MSC aging and enhancing immunomodulation: Novel strategies for cell-based therapies.Regenerative therapy · 2025Review
- Endometrial Stromal Senescence Mediates the Progression of Intrauterine Adhesions.International journal of molecular sciences · 2025Article
- Redox metabolism in cell senescence: focusing on contributions from the metabolomic field.Frontiers in molecular biosciences · 2025Review
- Cellular stress and epigenetic regulation in adult stem cells.Life science alliance · 2024Review
- Regulation of intestinal senescence during cholestatic liver disease modulates barrier function and liver disease progression.JHEP reports : innovation in hepatology · 2024Article
- Role of the GalNAc-galectin pathway in the healing of premature rupture of membranes.Molecular medicine (Cambridge, Mass.) · 2024Article
- Varied cellular abnormalities in thin vs. normal endometrium in recurrent implantation failure by single-cell transcriptomics.Reproductive biology and endocrinology : RB&E · 2024Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human endometrium-derived mesenchymal stem cells (hMESCs) enter the premature senescence under sublethal oxidative stress, however underlying mechanism remains unknown. Here, we showed that exogenous H2O2 induces a rapid phosphorylation and co-localization of ATM, H2A.X, 53BP1 leading to DNA damage response (DDR) activation. DDR was accompanied with nuclear translocation of p-p53 followed by up-regulation of p21Waf1 and the permanent hypophosphorylation of pRb. Additionally, the increased p38MAPK/MAPKAPK-2 activation persisted in H2O2-treated cells. We suggest that both p53/p21/pRb and p38MAPK/MAPKAPK-2 pathways are responsible for establishing an irreversible cell cycle arrest that is typical of senescence. The process of further stabilization of senescence required prolonged DDR signaling activation that was provided by the permanent ROS production which in turn was regulated by both p38MAPK and the increased functional mitochondria. To reverse senescence, the pharmacological inhibition of p38MAPK was performed. Cell treatment with SB203580 was sufficient to recover partially senescence phenotype, to block the ROS elevation, to decrease the mitochondrial function, and finally to rescue proliferation. Thus, suppression of the p38MAPK pathway resulted in a partial prevention of H2O2-induced senescence of hMESCs. The current study is the first to reveal the molecular mechanism of the premature senescence of hMESCs in response to oxidative stress.
Indexed as
Identifiers
What OpenQuestion holds
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.