ReviewEMBO reports2014
Senescence and apoptosis: dueling or complementary cell fates?
Review in EMBO reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 518 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
518 citing papers in PubMed, 1 synthesis or guideline pooled it, 871 citations in OpenAlex.
- Targeting cellular senescence with Traditional Chinese Medicine: advances in neurodegenerative disorder treatment.Frontiers in neurology · 2026Pooled it
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- p53 wild-type/low c-Myc-expressing ONS76 pediatric medulloblastoma cells become senescent after gamma-irradiation and can be eliminated by senolytic substances.Cell death discovery · 2026Article
- MLKL regulates intracellular trafficking of neutrophil elastase to promote lung epithelial cell senescence.American journal of respiratory cell and molecular biology · 2026Article
- The vicious cycle of SASP and inflammaging promotes aging and age-related diseases.Communications biology · 2026Review
- Targeting FEN1 disrupts EIF4A3-mediated MUC1-C autoregulation: a novel strategy to suppress lung adenocarcinoma progression.Cell death & disease · 2026Article
- Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer.Molecular oncology · 2026Review
- Article
- Biological Aging, Immune Phenotypes, and Susceptibility to COVID-19 and Sepsis: A Mendelian Randomization Study.Virus research · 2026Article
- Shared and disease-specific human brain vascular signatures in Alzheimer's disease, frontotemporal dementia, and Huntington's disease.bioRxiv : the preprint server for biology · 2026Article
- Exploring Stem Cell Based Senotherapeutic Strategies for Targeting Cellular Senescence in Brain Aging.Stem cell reviews and reports · 2026Review
- Non-Telomeric Role of RAP1 in Facilitating NF-κB Activation and Driving Hepatocellular Carcinoma Progression.IUBMB life · 2026Article
- p16 Beyond Senescence: Cancer Biology Lessons Applied to Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Review
- Endothelial progenitor cell susceptibility to DNA damaging and DDR-modulating compounds determines endothelial differentiation accuracy.Stem cell research & therapy · 2026Article
- Advanced drug delivery platforms targeting cellular senescence: A promising strategy for cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- Aucubin and Tanshinol from Bu-Shen-Huo-Xue-Fang (BSHXF) improve intervertebral disc degeneration through affecting nucleus pulposus cell.Journal of molecular histology · 2026Article
- Inhibition of Aurora B induces senescence and potentiates immunotherapy in hepatocellular carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Senolytic treatment with dasatinib and quercetin selectively improves cardiac autonomic balance in obesity.GeroScience · 2026Article
- Senescent endothelial cell-derived extracellular vesicles promote neoadjuvant chemoresistance in colorectal cancer via GPX4.Communications biology · 2026Article
458 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
5 authors at 3 institutions in 1 country.
Funding
Abstract
In response to a variety of stresses, mammalian cells undergo a persistent proliferative arrest known as cellular senescence. Many senescence-inducing stressors are potentially oncogenic, strengthening the notion that senescence evolved alongside apoptosis to suppress tumorigenesis. In contrast to apoptosis, senescent cells are stably viable and have the potential to influence neighboring cells through secreted soluble factors, which are collectively known as the senescence-associated secretory phenotype (SASP). However, the SASP has been associated with structural and functional tissue and organ deterioration and may even have tumor-promoting effects, raising the interesting evolutionary question of why apoptosis failed to outcompete senescence as a superior cell fate option. Here, we discuss the advantages that the senescence program may have over apoptosis as a tumor protective mechanism, as well as non-neoplastic functions that may have contributed to its evolution. We also review emerging evidence for the idea that senescent cells are present transiently early in life and are largely beneficial for development, regeneration and homeostasis, and only in advanced age do senescent cells accumulate to an organism's detriment.
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.