ArticlePharmaceuticals (Basel, Switzerland)2016
Evaluating the Role of p38 MAPK in the Accelerated Cell Senescence of Werner Syndrome Fibroblasts.
Article in Pharmaceuticals (Basel, Switzerland), 2016. 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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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.
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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
12 citing papers in PubMed, 21 citations in OpenAlex.
- Isolating and Validating Fibroblast-like Cells from the Skeletal Muscle of the Siamese Crocodile (Veterinary sciences · 2026Article
- Understanding cellular senescence: pathways involved, therapeutics and longevity aiding.Cell cycle (Georgetown, Tex.) · 2023Review
- Article
- The central role of DNA damage in immunosenescence.Frontiers in aging · 2023Review
- Activated microglia-induced neuroinflammatory cytokines lead to photoreceptor apoptosis in Aβ-injected mice.Journal of molecular medicine (Berlin, Germany) · 2021Article
- Crosstalk among DNA Damage, Mitochondrial Dysfunction, Impaired Mitophagy, Stem Cell Attrition, and Senescence in the Accelerated Ageing Disorder Werner Syndrome.Cytogenetic and genome research · 2021Review
- hTERT Transduction Extends the Lifespan of Primary Pediatric Low-Grade Glioma Cells While Preserving the Biological Response to NGF.Pathology oncology research : POR · 2021Article
- Senescent cells evade immune clearance via HLA-E-mediated NK and CD8Nature communications · 2019Article
- Cutaneous Manifestations of Scleroderma and Scleroderma-Like Disorders: a Comprehensive Review.Clinical reviews in allergy & immunology · 2017Review
- Osteosarcoma: Molecular Pathogenesis and iPSC Modeling.Trends in molecular medicine · 2017Review
- WRN Mutation Update: Mutation Spectrum, Patient Registries, and Translational Prospects.Human mutation · 2017Review
- Recent Advances in Understanding Werner Syndrome.F1000Research · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progeroid syndromes show features of accelerated ageing and are used as models for human ageing, of which Werner syndrome (WS) is one of the most widely studied. WS fibroblasts show accelerated senescence that may result from p38 MAP kinase activation since it is prevented by the p38 inhibitor SB203580. Thus, small molecule inhibition of p38-signalling may be a therapeutic strategy for WS. To develop this approach issues such as the in vivo toxicity and kinase selectivity of existing p38 inhibitors need to be addressed, so as to strengthen the evidence that p38 itself plays a critical role in mediating the effect of SB203580, and to find an inhibitor suitable for in vivo use. In this work we used a panel of different p38 inhibitors selected for: (1) having been used successfully in vivo in either animal models or human clinical trials; (2) different modes of binding to p38; and (3) different off-target kinase specificity profiles, in order to critically address the role of p38 in the premature senescence seen in WS cells. Our findings confirmed the involvement of p38 in accelerated cell senescence and identified p38 inhibitors suitable for in vivo use in WS, with BIRB 796 the most effective.
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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.