ReviewCurrent neuropharmacology2023
Neutrophil Extracellular Traps in Cerebral Ischemia/Reperfusion Injury: Friend and Foe.
Review in Current neuropharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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.
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Who cites it
47 citing papers in PubMed, 57 citations in OpenAlex.
- Electroacupuncture at Neiguan (PC6) and Shuigou (GV26) regulates microglial polarization and neuroinflammation through the cGAS-STING signaling pathway in ischemic stroke.IBRO neuroscience reports · 2026Article
- Review
- Targeting Neutrophil Extracellular Traps in Neuroinflammation: A Therapeutic Perspective on Neurodegenerative Diseases.Brain sciences · 2026Review
- Evolution of neutrophil extracellular traps in the pathology of stroke.Neural regeneration research · 2026Article
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- The relationship between inflammatory markers and the severity and prognosis of neurological dysfunction in stroke patients.BMC neurology · 2026Article
- Article
- GPNMB modulates neutrophil extracellular trap formation: therapeutic implications for ischemic stroke.Journal of neuroinflammation · 2026Article
- Neutrophils and Neutrophil Extracellular Traps in Hepatic Ischemia-Reperfusion Injury: Molecular Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Genistein-3'-sodium sulfonate improves neuroinflammation, blood-brain barrier function, and microglial activation after chronic cerebral hypoperfusion by regulating TGR5.Metabolic brain disease · 2026Article
- Extracellular vesicles: Revolutionizing targeted therapy for ischemic stroke.Acta pharmaceutica Sinica. B · 2026Review
- Cystatin B Attenuates Cerebral Ischemia Reperfusion Injury by Inhibiting the JAK2/STAT3 Signaling Pathway.CNS neuroscience & therapeutics · 2026Article
- Research advances on platelet glycoprotein VI in ischemic stroke.Thrombosis journal · 2026Review
- Danhong Injection Alleviates Blood-Brain Barrier Disruption Caused by Cerebral Ischemia-Reperfusion Injury inPharmaceuticals (Basel, Switzerland) · 2026Article
- Emerging Dual Roles of ALKBH5 in Ischemia-reperfusion Injury: Mechanisms and Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- Early symptom aggravation following ulnar nerve transposition for cubital tunnel syndrome: incidence, predictive factors, and threshold-based risk stratification.Neurosurgical review · 2026Article
- Research Trends in Neutrophil Extracellular Traps and Ischemia-Reperfusion Injury: A Dual-Database Bibliometric Analysis from 2013 to 2025.Journal of inflammation research · 2026Article
- The immunothrombosis pathway linking pulmonary disease to stroke and neurodegeneration: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Novel insights of acupuncture in ischemic stroke: orchestrating neuro-endocrine-immune network.Frontiers in immunology · 2026Review
- Cumulative inflammatory, coagulation, and metabolic abnormalities predict poor 90-day functional outcome after endovascular thrombectomy for large-vessel occlusion acute ischemic stroke.Frontiers in neurology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral ischemic injury, one of the leading causes of morbidity and mortality worldwide, triggers various central nervous system (CNS) diseases, including acute ischemic stroke (AIS) and chronic ischemia-induced Alzheimer's disease (AD). Currently, targeted therapies are urgently needed to address neurological disorders caused by cerebral ischemia/reperfusion injury (CI/RI), and the emergence of neutrophil extracellular traps (NETs) may be able to relieve the pressure. Neutrophils are precursors to brain injury following ischemic stroke and exert complicated functions. NETs extracellularly release reticular complexes of neutrophils, i.e., double-stranded DNA (dsDNA), histones, and granulins. Paradoxically, NETs play a dual role, friend and foe, under different conditions, for example, physiological circumstances, infection, neurodegeneration, and ischemia/reperfusion. Increasing evidence indicates that NETs exert anti-inflammatory effects by degrading cytokines and chemokines through protease at a relatively stable and moderate level under physiological conditions, while excessive amounts of NETs release (NETosis) irritated by CI/RI exacerbate the inflammatory response and aggravate thrombosis, disrupt the blood-brain barrier (BBB), and initiates sequential neuron injury and tissue damage. This review provides a comprehensive overview of the machinery of NETs formation and the role of an abnormal cascade of NETs in CI/RI, as well as other ischemia-induced neurological diseases. Herein, we highlight the potential of NETs as a therapeutic target against ischemic stroke that may inspire translational research and innovative clinical approaches.
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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.