ArticleThe Journal of clinical investigation2017
Molecular isoforms of high-mobility group box 1 are mechanistic biomarkers for epilepsy.
Article in The Journal of clinical investigation, 2017. 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 It has been retracted, and should not be counted.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 46 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 106 citations in OpenAlex.
- Elevation in plasma tRNA fragments precede seizures in human epilepsy.The Journal of clinical investigation · 2019Trial
- Obstructive sleep apnea and seizures: pathophysiological mechanisms and clinical implications: a narrative review.Sleep & breathing = Schlaf & Atmung · 2026Review
- Circulating microRNAs as Biomarkers of Various Forms of Epilepsy.Medical sciences (Basel, Switzerland) · 2025Article
- Circulating microRNAs from plasma as preclinical biomarkers of epileptogenesis and epilepsy.Scientific reports · 2024Article
- High Mobility Group Box 1 Levels as an Inflammatory Mediator in Bipolar Mania.Noro psikiyatri arsivi · 2024Article
- HMGB1 neuroimmune signaling and REST-G9a gene repression contribute to ethanol-induced reversible suppression of the cholinergic neuron phenotype.Molecular psychiatry · 2023Article
- Biomarkers of Drug Resistance in Temporal Lobe Epilepsy in Adults.Metabolites · 2023Article
- Article
- Serum Proteins Associated with Blood-Brain Barrier as Potential Biomarkers for Seizure Prediction.International journal of molecular sciences · 2022Article
- Amentoflavone Exerts Anti-Neuroinflammatory Effects by Inhibiting TLR4/MyD88/NF-Mediators of inflammation · 2022Article
- Cholinergic REST-G9a gene repression through HMGB1-TLR4 neuroimmune signaling regulates basal forebrain cholinergic neuron phenotype.Frontiers in molecular neuroscience · 2022Article
- Sleep Disruption Worsens Seizures: Neuroinflammation as a Potential Mechanistic Link.International journal of molecular sciences · 2021Review
- Recent Developments in Diagnosis of Epilepsy: Scope of MicroRNA and Technological Advancements.Biology · 2021Review
- Super-Refractory Status Epilepticus: Prognosis and Recent Advances in Management.Aging and disease · 2021Review
- Disulfide HMGB1 acts via TLR2/4 receptors to reduce the numbers of oligodendrocyte progenitor cells after traumatic injury in vitro.Scientific reports · 2021Article
- Proposal to optimize evaluation and treatment of Febrile infection-related epilepsy syndrome (FIRES): A Report from FIRES workshop.Epilepsia open · 2021Article
- The performance of the alarmin HMGB1 in pediatric diseases: From lab to clinic.Immunity, inflammation and disease · 2021Review
- Evaluation of serum high-mobility group box 1 concentration in dogs with epilepsy: A case-control study.Journal of veterinary internal medicine · 2020Article
- Inhibiting HMGB1-RAGE axis prevents pro-inflammatory macrophages/microglia polarization and affords neuroprotection after spinal cord injury.Journal of neuroinflammation · 2020Article
- Neurodegenerative pathways as targets for acquired epilepsy therapy development.Epilepsia open · 2020Review
Corrections and comments
- Retraction · 2019-04-08Falsification/Fabrication of Data · Miscommunication with/by Company/Institution · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · Unreliable Data · · Daniel J Antoine aka Daniel James Antoine;
- Retracted
Authors and funding
18 authors at 5 institutions in 4 countries.
Funding
Abstract
Approximately 30% of epilepsy patients do not respond to antiepileptic drugs, representing an unmet medical need. There is evidence that neuroinflammation plays a pathogenic role in drug-resistant epilepsy. The high-mobility group box 1 (HMGB1)/TLR4 axis is a key initiator of neuroinflammation following epileptogenic injuries, and its activation contributes to seizure generation in animal models. However, further work is required to understand the role of HMGB1 and its isoforms in epileptogenesis and drug resistance. Using a combination of animal models and sera from clinically well-characterized patients, we have demonstrated that there are dynamic changes in HMGB1 isoforms in the brain and blood of animals undergoing epileptogenesis. The pathologic disulfide HMGB1 isoform progressively increased in blood before epilepsy onset and prospectively identified animals that developed the disease. Consistent with animal data, we observed early expression of disulfide HMGB1 in patients with newly diagnosed epilepsy, and its persistence was associated with subsequent seizures. In contrast with patients with well-controlled epilepsy, patients with chronic, drug-refractory epilepsy persistently expressed the acetylated, disulfide HMGB1 isoforms. Moreover, treatment of animals with antiinflammatory drugs during epileptogenesis prevented both disease progression and blood increase in HMGB1 isoforms. Our data suggest that HMGB1 isoforms are mechanistic biomarkers for epileptogenesis and drug-resistant epilepsy in humans, necessitating evaluation in larger-scale prospective studies.
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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.