ReviewAge (Dordrecht, Netherlands)2015
Cellular senescence: from growth arrest to immunogenic conversion.
Review in Age (Dordrecht, Netherlands), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Psychological Stress and Cellular Aging in Cancer: A Meta-Analysis.Oxidative medicine and cellular longevity · 2019Pooled it
- Article
- Ferroptosis-Driven Senescence Loop as a Central Amplifier of Osteoarthritis Progression.Biomolecules & therapeutics · 2026Review
- The states of senescent cells.Biochemical Society transactions · 2025Review
- Harnessing Gasotransmitters to Combat Age-Related Oxidative Stress in Smooth Muscle and Endothelial Cells.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Cellular Senescence-Related Long Non-coding RNA Signatures Predict Prognosis in Juvenile Osteosarcoma.Phenomics (Cham, Switzerland) · 2024Article
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- Conofolidine: A Natural Plant Alkaloid That Causes Apoptosis and Senescence in Cancer Cells.Molecules (Basel, Switzerland) · 2024Article
- Rejuvenating aged microglia by p16Molecular neurodegeneration · 2024Article
- Anticipation and Verification of Dendrobium-Derived Nanovesicles for Skin Wound Healing Targets, Predicated Upon Immune Infiltration and Senescence.International journal of nanomedicine · 2024Article
- Review
- Inflammation and DNA damage: cause, effect or both.Nature reviews. Rheumatology · 2023Review
- Secretory Factors from Calcium-Sensing Receptor-Activated SW872 Pre-Adipocytes Induce Cellular Senescence and A Mitochondrial Fragmentation-Mediated Inflammatory Response in HepG2 Cells.International journal of molecular sciences · 2023Article
- Diabetes and Its Cardiovascular Complications: Potential Role of the Acetyltransferase p300.Cells · 2023Review
- Cellular Senescence in Acute and Chronic Wound Repair.Cold Spring Harbor perspectives in biology · 2022Review
- Schedule-Dependent Treatment Increases Chemotherapy Efficacy in Malignant Pleural Mesothelioma.International journal of molecular sciences · 2022Article
- Vascular contributions to cognitive impairment/dementia in diabetes: role of endothelial cells and pericytes.American journal of physiology. Cell physiology · 2022Review
- Nutritional Niches of Cancer Therapy-Induced Senescent Cells.Nutrients · 2022Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence was first reported in human fibroblasts as a state of stable in vitro growth arrest following extended culture. Since that initial observation, a variety of other phenotypic characteristics have been shown to co-associate with irreversible cell cycle exit in senescent fibroblasts. These include (1) a pro-inflammatory secretory response, (2) the up-regulation of immune ligands, (3) altered responses to apoptotic stimuli and (4) promiscuous gene expression (stochastic activation of genes possibly as a result of chromatin remodeling). Many features associated with senescent fibroblasts appear to promote conversion to an immunogenic phenotype that facilitates self-elimination by the immune system. Pro-inflammatory cytokines can attract and activate immune cells, the presentation of membrane bound immune ligands allows for specific recognition and promiscuous gene expression may function to generate an array of tissue restricted proteins that could subsequently be processed into peptides for presentation via MHC molecules. However, the phenotypes of senescent cells from different tissues and species are often assumed to be broadly similar to those seen in senescent human fibroblasts, but the data show a more complex picture in which the growth arrest mechanism, tissue of origin and species can all radically modulate this basic pattern. Furthermore, well-established triggers of cell senescence are often associated with a DNA damage response (DDR), but this may not be a universal feature of senescent cells. As such, we discuss the role of DNA damage in regulating an immunogenic response in senescent cells, in addition to discussing less established "atypical" senescent states that may occur independent of DNA damage.
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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.