ArticleThe EMBO journal2021
Neutrophils induce paracrine telomere dysfunction and senescence in ROS-dependent manner.
Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 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
132 citing papers in PubMed, 201 citations in OpenAlex.
- Trial
- Cytotoxic CD4Nature aging · 2026Article
- Single-Cell Mapping Identifies Aging-Associated Neutrophil Remodeling Across Multiple Organs.Aging cell · 2026Article
- Telomere-associated non-malignant pulmonary diseases: Pathogenic mechanisms and therapeutic strategies.Acta pharmaceutica Sinica. B · 2026Review
- Article
- The ageing immune system as a driver of systemic ageing.Nature reviews. Immunology · 2026Review
- Insights into the therapeutic strategies for aging and aging-associated diseases.Signal transduction and targeted therapy · 2026Review
- High altitude-mediated immune remodeling accelerates aging.Science advances · 2026Article
- The Role of Neutrophil, Monocyte and Macrophage Calprotectin and S100A12 in the Fibrotic Process.Biomolecules · 2026Review
- Aged murine bone marrow myeloid and mesenchymal cells develop unique senescence phenotypes.The Journal of clinical investigation · 2026Article
- Psoriasis-like disease prevents squamous skin tumor development by neutrophil-driven inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Host Aging Induces a Senescent-Like Phenotype in Neutrophils and Altered Transcriptional Responses to Streptococcus pneumoniae.Aging cell · 2026Article
- ROS Activated NETosis of Bone Marrow CD55Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fisetin-Mediated Topical Modulation of Senescent Cells in Skin Improves Wound Healing Dynamics in Diabetic Mice.Advances in wound care · 2026Article
- Identification and Validation of Liver Transplantation-Induced Acute Lung Injury Biomarkers Using a Bioinformatics and Experimental Approach.Annals of transplantation · 2026Article
- Tissue Immunometabolism in Autoimmunity.European journal of immunology · 2026Review
- Characteristic Changes in the Immune Landscape of Aging Liver: From Basic Mechanism to Clinical Transformation.Journal of immunology research · 2026Review
- Persistent pneumococcal colonisation in antiretroviral-treated HIV infection is associated with nasal inflammation.Nature communications · 2025Article
- Endothelial senescent-cell-specific clearance alleviates metabolic dysfunction in obese mice.Cell metabolism · 2025Article
- Distinct senotypes in p16- and p21-positive cells across human and mouse aging tissues.The EMBO journal · 2025Article
72 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
37 authors at 11 institutions in 5 countries.
Funding
Abstract
Cellular senescence is characterized by an irreversible cell cycle arrest as well as a pro-inflammatory phenotype, thought to contribute to aging and age-related diseases. Neutrophils have essential roles in inflammatory responses; however, in certain contexts their abundance is associated with a number of age-related diseases, including liver disease. The relationship between neutrophils and cellular senescence is not well understood. Here, we show that telomeres in non-immune cells are highly susceptible to oxidative damage caused by neighboring neutrophils. Neutrophils cause telomere dysfunction both in vitro and ex vivo in a ROS-dependent manner. In a mouse model of acute liver injury, depletion of neutrophils reduces telomere dysfunction and senescence. Finally, we show that senescent cells mediate the recruitment of neutrophils to the aged liver and propose that this may be a mechanism by which senescence spreads to surrounding cells. Our results suggest that interventions that counteract neutrophil-induced senescence may be beneficial during aging and age-related disease.
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.