ReviewInternational journal of molecular sciences2021
Mechanisms and Regulation of Cellular Senescence.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 238 papers, 2 of them syntheses 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
238 citing papers in PubMed, 2 syntheses or guidelines pooled it, 362 citations in OpenAlex.
- MicroRNAs and Cellular Senescence in Melanoma: An Underexplored Link to Tumor Progression-A Systematic Review with Bioinformatics Analyses.International journal of molecular sciences · 2026Pooled it
- Broad repression of DNA repair genes in senescent cells identified by integration of transcriptomic data.Nucleic acids research · 2025Pooled it
- Co-administration of vitamin D and N-acetylcysteine to modulate immunosenescence in older adults with vitamin D deficiency: a randomized clinical trial.Frontiers in immunology · 2025Trial
- Stress granules and RNA-binding proteins in cellular senescence: a modular perspective on stress adaptation and inflammation.Molecular biology reports · 2026Review
- Senescent Cell Heterogeneity: Tissue-Dependent Signatures and Age Dynamics Revealed by Human scRNA-Seq Data.International journal of molecular sciences · 2026Article
- Conditional Senescence and Longevity Mechanisms in Early-Branching Metazoans: Insights fromCurrent issues in molecular biology · 2026Article
- LSD1-mediated demethylation of the DNA damage response factor ATM promotes senescence and organ aging.The Journal of clinical investigation · 2026Article
- Palmitoylethanolamide and Luteolin in Brain Aging and Cognitive Decline: Biological Rationale and Current Evidence.Nutrients · 2026Review
- The Gut Microbiome as a Mechanistic Link Between the Planetary Health Diet and Healthy Aging.Nutrients · 2026Review
- Formononetin attenuates cellular senescence through a FOS-mediated mechanism.Biogerontology · 2026Article
- Senolytic Therapy as a Preventive Strategy for Spine Degeneration and Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A prognostic senescence-related long non-coding RNA signature identifies cold and hot tumors of stomach adenocarcinoma.Oncology letters · 2026Article
- A Cell-Based Therapeutic Strategy for Stress Urinary Incontinence: Functional and Molecular Evidence from Decidua-Derived Mesenchymal Stromal Cells.International journal of molecular sciences · 2026Article
- Distinct roles of COPI proteins attenuated in cell senescence.Science advances · 2026Article
- Quercetin Mitigates Oxidative Stress-Induced Premature Senescence in SH-SY5Y Neuronal-like Cells.International journal of molecular sciences · 2026Article
- Article
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Review
- METTL3/YTHDF1 drives M1 macrophage polarization and aggravates ulcerative colitis progression by regulating m6A modification of SerpinB5 mRNA and FBXO32-dependent NF-κB pathway.Journal of gastroenterology · 2026Article
- Dietary Polyphenols in Aging: A Systems-Level Perspective on Mitochondrial Quality Control and Microbiome Interactions.International journal of molecular sciences · 2026Review
178 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence entails a state of an essentially irreversible proliferative arrest in which cells remain metabolically active and secrete a range of pro-inflammatory and proteolytic factors as part of the senescence-associated secretory phenotype. There are different types of senescent cells, and senescence can be induced in response to many DNA damage signals. Senescent cells accumulate in different tissues and organs where they have distinct physiological and pathological functions. Despite this diversity, all senescent cells must be able to survive in a nondividing state while protecting themselves from positive feedback loops linked to the constant activation of the DNA damage response. This capacity requires changes in core cellular programs. Understanding how different cell types can undergo extensive changes in their transcriptional programs, metabolism, heterochromatin patterns, and cellular structures to induce a common cellular state is crucial to preventing cancer development/progression and to improving health during aging. In this review, we discuss how senescent cells continuously evolve after their initial proliferative arrest and highlight the unifying features that define the senescent state.
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.