ArticleImmunology2017
Aging-related Atg5 defect impairs neutrophil extracellular traps formation.
Article in Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
What it found
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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
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Role of Neutrophils on the Ocular Surface.International journal of molecular sciences · 2021Pooled it
- Neutrophil extracellular traps in tumor progression: from mechanistic insights and regulatory factors to clinical detection and diagnosis.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Article
- Immunosenescence and Cancer: Cellular Aging Programs That Reshape Antitumor Immunity.Immune network · 2026Review
- Age affects the immune system more than a moderate surgical trauma and anesthesia.Scientific reports · 2025Article
- Neutrophil Extracellular Traps (NETs) as a Potential Target for Anti-Aging: Role of Therapeutic Apheresis.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2025Review
- Sex Differences in Immune Responses to Infectious Diseases: The Role of Genetics, Hormones, and Aging.Diseases (Basel, Switzerland) · 2025Review
- Neutrophils: a new target for postoperative cognitive dysfunction.Apoptosis : an international journal on programmed cell death · 2025Review
- Extracellular Traps in Inflammation: Pathways and Therapeutic Targets.Life (Basel, Switzerland) · 2025Review
- The inducible role of autophagy in cell death: emerging evidence and future perspectives.Cell communication and signaling : CCS · 2025Review
- The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases.MedComm · 2025Review
- Metabolic reprogramming in cancer and senescence.MedComm · 2025Review
- Increased cell-free DNA in CSF and serum of hip fracture patients with delirium.Brain communications · 2025Article
- Autophagy-mediated regulation of neutrophil inflammatory responses and its relevance to central nervous system diseases.Frontiers in aging neuroscience · 2025Review
- Suppression of Inflammation by Si Miao San in Experimental Rheumatoid Arthritis Through Modulation of the AKT/ROS/Autophagy Axis.Journal of inflammation research · 2025Article
- Double-Responsive Macrophage-Derived Exosomes Alleviate Acute Lung Injury.Biomaterials research · 2025Article
- Cellular senescence: A new perspective on the suppression of periodontitis (Review).Molecular medicine reports · 2024Review
- Immunosenescence: Aging and Immune System Decline.Vaccines · 2024Review
- Dying to Defend: Neutrophil Death Pathways and their Implications in Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- The emerging role of neutrophil extracellular traps in ulcerative colitis.Frontiers in immunology · 2024Review
5 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
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Formation of neutrophil extracellular traps (NETs) is an important function of the innate immune system against infections. It has been proven that aging dysregulates immunity and impairs neutrophil function. However, the influence of aging on the ability to produce NETs has yet to be fully addressed. In this study, we tested the hypothesis that a lower level of autophagy in neutrophils from aged mice was responsible for the decrease in NET formation. We demonstrated that a broad range of Toll-like receptor 2 (TLR2) ligands could efficiently induce reactive oxygen species (ROS) -dependent NET release in young mice, but not in aged ones. We further explored that the difference between young and aged mice in TLR2 ligand-induced NETosis is the result of an Atg5 defect and subsequent impaired autophagy. Furthermore, we found that lower autophagy capacity led to not only reduced NET formation, but also increased apoptosis. Our results suggest an important role of Atg5 and autophagy in maintaining the function of NETs formation in response to infection and in regulating neutrophil death. Targeting autophagy-promoted NETs may present a therapeutic strategy to improve infection defence in an aged population.
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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.