ReviewArchives of toxicology2023
c-Jun N-terminal kinase signaling in cellular senescence.
Review in Archives of toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- The Association Between Serum Gamma-Glutamyl Transferase and Gastrointestinal Cancer Risk: A Systematic Review and Meta-Analysis.Cancer medicine · 2025Pooled it
- IGFBP5 alleviates periodontitis by reversing human dental follicle stem cell senescence via the non-canonical Wnt pathway.International journal of oral science · 2026Article
- Review
- c-Jun in neurodegeneration: A key transcriptional regulator with therapeutic implications.Molecular therapy. Nucleic acids · 2026Review
- Article
- The RNA-binding protein SRSF3 controls epicardial formation by regulating splicing and proliferation.Development (Cambridge, England) · 2026Article
- Harnessing Natural Extracellular Vesicles to Combat Age-Related Diseases: From Aging Drivers to Therapeutic Opportunities.International journal of nanomedicine · 2026Review
- Carnosic Acid Mediates Production of Reactive Oxygen Species to Regulate Mitogen-Activated Protein Kinase Pathway Phosphorylation and Induce Apoptosis in Human Breast Cancer Cells.Cancer medicine · 2026Article
- Anti-senescence and anti-apoptotic effects of immatureToxicological research · 2025Article
- IFI30 Knockdown Inhibits ESCC Progression by Promoting Apoptosis and Senescence via Activation of JNK and P21/P16 Pathways.Thoracic cancer · 2025Article
- Digital spatial profiling identifies phospho-JNK as a biomarker for early risk stratification of aggressive prostate cancer.Frontiers in oncology · 2025Article
- Immune regulation and the tumor microenvironment in anti-PD-1/PDL-1 and anti-CTLA-4 therapies for cancer immune evasion: A bibliometric analysis.Human vaccines & immunotherapeutics · 2024Review
- Article
- Article
- Common ground on immune infiltration landscape and diagnostic biomarkers in diabetes-complicated atherosclerosis: an integrated bioinformatics analysis.Frontiers in endocrinology · 2024Article
- c-Jun N-terminal kinase signaling in aging.Frontiers in aging neuroscience · 2024Review
- Neuroprotective Effects of Empagliflozin Against Methamphetamine-Induced Withdrawal Syndrome in Mice: Involvement of Bdnf, Tlr4, and JNK Signaling Pathways and Oxidative Stress Biomarkers.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence leads to decreased tissue regeneration and inflammation and is associated with diabetes, neurodegenerative diseases, and tumorigenesis. However, the mechanisms of cellular senescence are not fully understood. Emerging evidence has indicated that c-Jun N-terminal kinase (JNK) signaling is involved in the regulation of cellular senescence. JNK can downregulate hypoxia inducible factor-1α to accelerate hypoxia-induced neuronal cell senescence. The activation of JNK inhibits mTOR activity and triggers autophagy, which promotes cellular senescence. JNK can upregulate the expression of p53 and Bcl-2 and accelerates cancer cell senescence; however, this signaling also mediates the expression of amphiregulin and PD-LI to achieve cancer cell immune evasion and prevents their senescence. The activation of JNK further triggers forkhead box O expression and its target gene Jafrac1 to extend the lifespan of Drosophila. JNK can also upregulate the expression of DNA repair protein poly ADP-ribose polymerase 1 and heat shock protein to delay cellular senescence. This review discusses recent advances in understanding the function of JNK signaling in cellular senescence and includes a comprehensive analysis of the molecular mechanisms underlying JNK-mediated senescence evasion and oncogene-induced cellular senescence. We also summarize the research progress in anti-aging agents that target JNK signaling. This study will contribute to a better understanding of the molecular targets of cellular senescence and provides insights into anti-aging, which may be used to develop drugs for the treatment of aging-related diseases.
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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.