ArticleCell2008
Chemokine signaling via the CXCR2 receptor reinforces senescence.
Article in Cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,013 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
1,013 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,764 citations in OpenAlex.
- Consequences of Aging on Bone.Aging and disease · 2023Pooled it
- Effect of nicotinamide riboside on airway inflammation in COPD: a randomized, placebo-controlled trial.Nature aging · 2024Trial
- Cellular senescence: six decades of discovery and reinvention.The EMBO journal · 2026Review
- Senolytics dasatinib and quercetin in metabolic dysfunction-associated steatohepatitis: a proof-of-principle randomized, controlled trial.Nature metabolism · 2026Article
- Accelerated aging in schizophrenia: integrating epigenetic clocks, telomere dynamics, senescence-associated secretory phenotype, and oxidative stress.European archives of psychiatry and clinical neuroscience · 2026Review
- Article
- Peroxisomal Import Stress Drives Cellular Senescence through SCAF1-dependent Suppression of Mitoribosome Biogenesis.bioRxiv : the preprint server for biology · 2026Article
- The vicious cycle of SASP and inflammaging promotes aging and age-related diseases.Communications biology · 2026Review
- The intersection of chemokine signaling with the hallmarks of cancer in glioblastoma.Journal of neuro-oncology · 2026Review
- 3'UTR-directed, kinase-proximal mRNA decay inhibits C/EBPβ phosphorylation/activation to suppress senescence in tumor cells.iScience · 2026Article
- Immune surveillance and immune evasion of senescent cells.Nature reviews. Immunology · 2026Review
- Royal jelly suppresses senescence-associated secretory phenotype in senescent human epidermal keratinocytes.Molecular biology reports · 2026Article
- Targeting YAP1-Mediated Tubular Cell Senescence to Attenuate Maladaptive Repair and Fibrotic Transition After Acute Kidney Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Epigenetic dynamics of cellular senescence: From mechanistic insights to precision senotherapy.Chinese medical journal · 2026Review
- Limitations of the p16-3MR mouse model for detecting and eliminating senescent cells.EMBO reports · 2026Article
- Review
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Cellular Senescence and the SASP in HFpEF: Pathogenic Mechanisms and Therapeutic Targeting.International journal of molecular sciences · 2026Review
- Cellular Senescence in Idiopathic Pulmonary Fibrosis: Molecular Mechanisms, Pathogenic Networks, and Emerging Therapeutic Targets.Diseases (Basel, Switzerland) · 2026Review
- A conserved regulatory architecture stabilizes cellular senescence across distinct triggers in human fibroblasts.GeroScience · 2026Article
953 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
16 authors at 3 institutions in 3 countries.
Funding
Abstract
Cells enter senescence, a state of stable proliferative arrest, in response to a variety of cellular stresses, including telomere erosion, DNA damage, and oncogenic signaling, which acts as a barrier against malignant transformation in vivo. To identify genes controlling senescence, we conducted an unbiased screen for small hairpin RNAs that extend the life span of primary human fibroblasts. Here, we report that knocking down the chemokine receptor CXCR2 (IL8RB) alleviates both replicative and oncogene-induced senescence (OIS) and diminishes the DNA-damage response. Conversely, ectopic expression of CXCR2 results in premature senescence via a p53-dependent mechanism. Cells undergoing OIS secrete multiple CXCR2-binding chemokines in a program that is regulated by the NF-kappaB and C/EBPbeta transcription factors and coordinately induce CXCR2 expression. CXCR2 upregulation is also observed in preneoplastic lesions in vivo. These results suggest that senescent cells activate a self-amplifying secretory network in which CXCR2-binding chemokines reinforce growth arrest.
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.