ReviewThe Journal of clinical investigation2018
Mechanisms and functions of cellular senescence.
Review in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 729 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
729 citing papers in PubMed, 1,118 citations in OpenAlex.
- Combining bioinformatics and machine learning to analyze and validate sepsis-related cell senescence genes and potential drugs.Renal failure · 2026Article
- Is Cellular Senescence a Biological Feature of Long COVID? A Transcriptomic Analysis Across Comparative Postacute Sequelae Phenotypes.The Journal of infectious diseases · 2026Article
- Fusobacterium nucleatum promotes senescence of human oral mucosa fibroblasts via the Wnt5A/mTOR pathway.Odontology · 2026Article
- Therapy-Induced Senescence in Cancer Treatment Resistance: Mechanisms, Evidence, and Translational Opportunities.Cancers · 2026Review
- Aqueous Extract ofPharmaceuticals (Basel, Switzerland) · 2026Article
- Palmitoylethanolamide and Luteolin in Brain Aging and Cognitive Decline: Biological Rationale and Current Evidence.Nutrients · 2026Review
- Evolutionary genetics of ageing.Nature reviews. Genetics · 2026Review
- Rethinking Senescence Hallmarks in the Brain: Lessons From Peripheral Tissues and Challenges in Defining Neuronal Senescence.Aging cell · 2026Review
- Oncoviruses at the Crossroads of Ageing and Cancer: Molecular Mechanisms and Key Signalling Pathways.Reviews in medical virology · 2026Review
- APC/C-CDH1 suppresses AROS-mediated protection against DNA damage-induced senescence by ubiquitination.BMB reports · 2026Article
- Direct targeting of ORAI1 by ginsenoside Rg3 modulates calcium signaling and senescence-associated AMPK-NRF2 activation.Journal of ginseng research · 2026Article
- NADAging cell · 2026Article
- CD38-activated macrophages drive age-related placental senescence by depleting NADNature communications · 2026Article
- Mitochondrial Redox Failure Links Senescence-like Foam Cell Stress to Ferroptosis and Plaque Non-Resolution in Atherosclerosis.Antioxidants (Basel, Switzerland) · 2026Review
- Particulate Matter-Induced Skin Injury: A Dual-Pathway AhR-Nrf2 Framework for Epidermal Homeostasis and Therapeutic Targeting.International journal of molecular sciences · 2026Review
- 3'UTR-directed, kinase-proximal mRNA decay inhibits C/EBPβ phosphorylation/activation to suppress senescence in tumor cells.iScience · 2026Article
- Senolytics Reverse PMCardiovascular toxicology · 2026Article
- Article
- DNA Sensing Pathways in Innate Immunity: Implications for Alzheimer's Disease Progression and Therapy.Molecular neurobiology · 2026Review
- Article
669 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Cellular senescence is a highly stable cell cycle arrest that is elicited in response to different stresses. By imposing a growth arrest, senescence limits the replication of old or damaged cells. Besides exiting the cell cycle, senescent cells undergo many other phenotypic alterations such as metabolic reprogramming, chromatin rearrangement, or autophagy modulation. In addition, senescent cells produce and secrete a complex combination of factors, collectively referred as the senescence-associated secretory phenotype, that mediate most of their non-cell-autonomous effects. Because senescent cells influence the outcome of a variety of physiological and pathological processes, including cancer and age-related diseases, pro-senescent and anti-senescent therapies are actively being explored. In this Review, we discuss the mechanisms regulating different aspects of the senescence phenotype and their functional implications. This knowledge is essential to improve the identification and characterization of senescent cells in vivo and will help to develop rational strategies to modulate the senescence program for therapeutic benefit.
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.