ReviewGenes & development2014
Cellular senescence and its effector programs.
Review in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 500 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
500 citing papers in PubMed.
- Bone marrow mesenchymal stem cells are functionally remodeled after complete remission of acute myeloid leukemia.Journal of translational internal medicine · 2026Article
- Cellular senescence: the "hidden driver" in chronic inflammatory skin disorders.Immunity & ageing : I & A · 2026Review
- What Do We Know About Immune System Aging from Human and Animal Studies?International journal of molecular sciences · 2026Review
- Towards a context-aware framework for cellular senescence.Biogerontology · 2026Review
- Single-cell and spatial transcriptome analysis reveals the potential therapeutic targets for testicular sex cord-stromal cell tumor.Biomarker research · 2026Article
- Ginger Bioactives as Multi-Target Therapeutics: Mechanisms, Delivery Innovation, and Human Health Impact.Nutrients · 2026Review
- Chondrocyte Senescence in Osteoarthritis: Potential Targets and Pharmacological Interventions.Cartilage · 2026Article
- BAP1 Loss Induces Senescence and Enhances the Response to Radiation Therapy and Senolytics.bioRxiv : the preprint server for biology · 2026Article
- Phosphorylation of CBX8 by PKD1 suppresses PRC1 activity and promotes cell senescence.Oncogene · 2026Article
- Tumor-associated macrophages educated by IGSF9 exhibit a senescence-associated secretory phenotype to promote tumor immune escape.Journal for immunotherapy of cancer · 2026Article
- Chimeric Antigen Receptor T Cells as Living Therapeutics Targeting Senescence and Age-Related Diseases.Research (Washington, D.C.) · 2026Review
- GDF15 participates in epithelial cell senescence in radiation-induced lung injury through the ERK1/2-p16 signaling pathway.PloS one · 2026Article
- Physical exercise therapy as an anti-aging strategy for osteosarcopenia: a narrative review.Frontiers in aging · 2026Review
- Cellular senescence in cancer immunology and potential therapeutic strategy.Frontiers in oncology · 2026Review
- Transcriptional regulation in cardiovascular aging.Frontiers in cardiovascular medicine · 2026Review
- Elucidate senescence-related gene signature and immune infiltration landscape in abdominal aortic aneurysm.PloS one · 2026Article
- Neutrophil extracellular traps-triggered hepatocellular senescence exacerbates lipotoxicity in non-alcoholic steatohepatitis.Journal of advanced research · 2026Article
- MRTF-dependent cytoskeletal dynamics drive efficient cell cycle progression.Journal of cell science · 2025Article
- Further characterisation of immortalised human lymphatic endothelial cells to explore their transcriptomic profile and VEGFC response.Scientific reports · 2025Article
- 5'tiRNA-Glu-TTC targets TRPV3 and activates the PI3K/AKT signaling pathway to modulate skin photoaging.Non-coding RNA research · 2025Article
440 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
4 authors.
Funding
Abstract
Cellular senescence is a stress response that accompanies stable exit from the cell cycle. Classically, senescence, particularly in human cells, involves the p53 and p16/Rb pathways, and often both of these tumor suppressor pathways need to be abrogated to bypass senescence. In parallel, a number of effector mechanisms of senescence have been identified and characterized. These studies suggest that senescence is a collective phenotype of these multiple effectors, and their intensity and combination can be different depending on triggers and cell types, conferring a complex and diverse nature to senescence. Series of studies on senescence-associated secretory phenotype (SASP) in particular have revealed various layers of functionality of senescent cells in vivo. Here we discuss some key features of senescence effectors and attempt to functionally link them when it is possible.
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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.