ArticleFEBS open bio2020
ROCK inhibition modulates the senescence-associated secretory phenotype (SASP) in oral keratinocytes.
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 31 citations in OpenAlex.
- AMF30a promotes survival and function of human corneal endothelial cells by regulating TGF-β/ROCK/HIPPO pathway.Scientific reports · 2025Article
- Therapeutic Efficacy of Small Extracellular Vesicles Loaded with ROCK Inhibitor in Parkinson's Disease.Pharmaceutics · 2025Article
- Suppressing the Aging Phenotype of Mesenchymal Stromal Cells: Are We Ready for Clinical Translation?Biomedicines · 2024Review
- Cellular senescence and metabolic reprogramming: Unraveling the intricate crosstalk in the immunosuppressive tumor microenvironment.Cancer communications (London, England) · 2024Review
- Osteopontin Rejuvenates Senescent Adipose-Derived Stem Cells and Restores their Bone Tissue Regenerative Function.Stem cell reviews and reports · 2024Article
- High salt diet accelerates skin aging in wistar rats: an 8-week investigation of cell cycle inhibitors, SASP markers, and oxidative stress.Frontiers in bioengineering and biotechnology · 2024Article
- Decoding the Human Epidermal Complexity at Single-Cell Resolution.International journal of molecular sciences · 2023Review
- Cellular rejuvenation: molecular mechanisms and potential therapeutic interventions for diseases.Signal transduction and targeted therapy · 2023Review
- Article
- Aging and oral squamous cell carcinoma development: the role of cellular senescence.Frontiers in oral health · 2023Review
- Senescence-associated secretory phenotype and its impact on oral immune homeostasis.Frontiers in immunology · 2022Review
- Overcoming the senescence-associated secretory phenotype (SASP): a complex mechanism of resistance in the treatment of cancer.Molecular oncology · 2021Review
- Review
- Skin Aging, Cellular Senescence and Natural Polyphenols.International journal of molecular sciences · 2021Review
- Article
- Inflammatory Mediators in Oral Cancer: Pathogenic Mechanisms and Diagnostic Potential.Frontiers in oral health · 2021Review
- The Contribution of Physiological and Accelerated Aging to Cancer Progression Through Senescence-Induced Inflammation.Frontiers in oncology · 2021Review
- The emerging role of cellular senescence in complications of COVID-19.Cancer treatment and research communications · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescent cells accumulate in different organs and develop a senescence-associated secretory phenotype (SASP), associated with the development of age-related pathologies. The constitution of the SASP varies among cell types and with the method of senescence induction; nevertheless, there is substantial overlap among SASPs, especially the presence of pro-inflammatory cytokines such as IL-1β, IL-1α, IL-6 and IL-8. These cytokines are highly conserved among SASPs and are implicated in the development of several cancers. Here, we report that ROCK inhibition by Y-27632 reduces levels of IL-1α, IL-1β, IL-6 and IL-8 secreted by senescent normal and dysplastic oral keratinocytes without affecting the permanent cell growth arrest. The data indicate some inflammatory genes downregulated by Y-27632 remain downregulated even after repeated passage in the absence of Y-27632. We propose ROCK kinase inhibition as a novel alternative to current strategies to modulate the inflammatory components of the SASP, without compromising the permanent cell growth arrest. This observation potentially has wide clinical applications, given the involvement of senescence in cancer and a wide range of age-related disease. It also suggests care should be exercised when using Y-27632 to facilitate cell expansion of primary cells, as its effects on gene expression are not entirely reversible.
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.