ArticleTranslational stroke research2019
Release of IL-6 After Stroke Contributes to Impaired Cerebral Autoregulation and Hippocampal Neuronal Necrosis Through NMDA Receptor Activation and Upregulation of ET-1 and JNK.
Article in Translational stroke research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 35 papers.
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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.
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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
35 citing papers in PubMed, 61 citations in OpenAlex.
- Different light color temperatures in the morning on the effectiveness of rehabilitation training in patients with ischemic stroke: a prospective, single-center, randomized controlled clinical trial.Journal of neuroengineering and rehabilitation · 2025Trial
- Serum inflammatory cytokines predict 90-day outcome after endovascular treatment in acute ischemic stroke.Frontiers in neurology · 2026Article
- The interaction of tPA with NMDAR1 drives neuroinflammation and neurodegeneration in α-synuclein-mediated neurotoxicity.Journal of neuroinflammation · 2025Article
- Biomimetic astrocyte cell membrane-fused nanovesicles for protecting neurovascular units in hypoxic ischemic encephalopathy.Journal of nanobiotechnology · 2024Article
- Associations of Rheumatoid Factor, Rheumatoid Arthritis, and Interleukin-6 Inhibitor with the Prognosis of Ischemic Stroke: a Prospective Multicenter Cohort Study and Mendelian Randomization Analysis.Translational stroke research · 2024Article
- Therapeutic effect and psychological impact of aspirin plus edaravone on patients with cerebral infarction.World journal of psychiatry · 2024Article
- Bioinformatics analysis and experimental validation revealed that Paeoniflorigenone effectively mitigates cerebral ischemic stroke by suppressing oxidative stress and inflammation.Scientific reports · 2024Article
- Quercetin Protects Against Global Cerebral ischemia‒reperfusion Injury by Inhibiting Microglial Activation and Polarization.Journal of inflammation research · 2024Article
- Investigating the Potential Mechanisms and Therapeutic Targets of Inflammatory Cytokines in Post-stroke Depression.Molecular neurobiology · 2024Review
- Sanhua decoction: Current understanding of a traditional herbal recipe for stroke.Frontiers in neuroscience · 2023Review
- A GP130-Targeting Small Molecule, LMT-28, Reduces LPS-Induced Bone Resorption around Implants in Diabetic Models by Inhibiting IL-6/GP130/JAK2/STAT3 Signaling.Mediators of inflammation · 2023Article
- Article
- Network pharmacology andPharmaceutical biology · 2022Article
- Diabetes and the treatment of ischemic stroke.Journal of diabetes and its complications · 2022Review
- Targeting NMDA Receptors at the Neurovascular Unit: Past and Future Treatments for Central Nervous System Diseases.International journal of molecular sciences · 2022Review
- Old but Still Hot Target, Glutamate-Mediated Neurotoxicity in Stroke.Translational stroke research · 2022Article
- Interleukins and Ischemic Stroke.Frontiers in immunology · 2022Review
- Propofol ameliorates ischemic brain injury by blocking TLR4 pathway in mice.Translational neuroscience · 2022Article
- SOCS1/JAK2/STAT3 axis regulates early brain injury induced by subarachnoid hemorrhage via inflammatory responses.Neural regeneration research · 2021Article
- Regulation of the Cerebral Circulation During Development.Comprehensive Physiology · 2021Article
Corrections and comments
- Retraction · 2024-06-06Concerns/Issues about Data · Duplication of/in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Unreliable Data · · William M Armstead has ORI finding of misconduct :https://ori.hhs.gov/content/case-summary-armstead-william-m;
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sole FDA-approved drug treatment for ischemic stroke is tissue-type plasminogen activator (tPA). However, upregulation of JNK mitogen-activated protein kinase (MAPK) and endothelin 1 (ET-1) by tPA after stroke contributes to impaired cerebrovascular autoregulation. Wild-type (wt) tPA can bind to the lipoprotein-related receptor (LRP), which mediates vasodilation, or NMDA receptors (NMDA-Rs), exacerbating vasoconstriction. Elevations in IL-6, a marker of inflammation that accompanies stroke, are reported to be an adverse prognostic factor. We hypothesized that IL-6 released into CSF after stroke by wt-tPA through activation of NMDA-Rs and upregulation of ET-1 and JNK contribute to impairment of cerebrovascular autoregulation and increased histopathology. Results show that IL-6 was increased post stroke in pigs, which was increased further by wt-tPA. Co-administration of the IL-6 antagonist LMT-28 with wt-tPA prevented impairment of cerebrovascular autoregulation and necrosis of hippocampal cells. wt-tPA co-administered with the JNK inhibitor SP 600125 and the ET-1 antagonist BQ 123 blocked stroke-induced elevation of IL-6. Co-administration of LMT-28 with wt-tPA blocked the augmentation of JNK and ET-1 post stroke. In conclusion, IL-6 released after stroke, which is enhanced by wt-tPA through activation of NMDA-Rs and upregulation of ET-1 and JNK, impairs cerebrovascular autoregulation and increases histopathology. Strategies that promote fibrinolysis while limiting activation of NMDA-Rs and upregulation of IL-6 may improve the benefit/risk ratio compared to wt-tPA in treatment of stroke.
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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.