ReviewFrontiers in cellular neuroscience2020
The Roles of High Mobility Group Box 1 in Cerebral Ischemic Injury.
Review in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Association between circulating inflammatory biomarkers and functional outcome or perihaematomal oedema after ICH: a systematic review & meta-analysis.Wellcome open research · 2023Pooled it
- The mechanisms by which hypothalamic neuroinflammation induced by neonatal cerebral ischemia-hypoxia leads to decreased thymic function via the HPA axis.Cell & bioscience · 2026Article
- Microglia-neuron communication in ischemic stroke: from homeostatic signaling to pathological remodeling and therapeutic targeting.Frontiers in molecular biosciences · 2026Review
- Interaction Between Neutrophils and Elements of the Blood-Brain Barrier in the Context of Multiple Sclerosis and Ischemic Stroke.International journal of molecular sciences · 2025Review
- High-Mobility Group Box-1 as a Predictor for Malignant Brain Edema Following Mechanical Thrombectomy in Acute Ischemic Stroke Patients.International journal of general medicine · 2025Article
- From copper homeostasis to cuproptosis: a new perspective on CNS immune regulation and neurodegenerative diseases.Frontiers in neurology · 2025Review
- Neuroprotective Potential of Glycyrrhizic Acid in Ischemic Stroke: Mechanisms and Therapeutic Prospects.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024Review
- Modulation of Abundance and Location of High-Mobility Group Box 1 in Human Microglia and Macrophages under Oxygen-Glucose Deprivation.ACS pharmacology & translational science · 2024Article
- Calycosin Ameliorates Neuroinflammation via TLR4-Mediated Signal Following Cerebral Ischemia/Reperfusion Injury in vivo and in vitro.Journal of inflammation research · 2024Article
- Vesicular HMGB1 release from neurons stressed with spreading depolarization enables confined inflammatory signaling to astrocytes.Journal of neuroinflammation · 2023Article
- Review
- Design of an Anti-HMGB1 Synthetic Antibody forJournal of the American Chemical Society · 2023Article
- Astroglial Hmgb1 regulates postnatal astrocyte morphogenesis and cerebrovascular maturation.Nature communications · 2023Article
- Cytokine Levels and Severity of Illness Scoring Systems to Predict Mortality in COVID-19 Infection.Healthcare (Basel, Switzerland) · 2023Article
- Galantamine ameliorates hyperoxia-induced brain injury in neonatal mice.Frontiers in neuroscience · 2023Article
- Neutrophil Extracellular Traps in Cerebral Ischemia/Reperfusion Injury: Friend and Foe.Current neuropharmacology · 2023Review
- HMGB1 promotes Ox-LDL-induced endothelial cell damage by inhibiting PI3K/Akt signaling pathway.BMC cardiovascular disorders · 2022Article
- Astrocytic CD24 Protects Neuron from Recombinant High-Mobility Group Box 1 Protein(rHMGB1)-Elicited Neuronal Injury.Brain sciences · 2022Article
- Haptoglobin Regulates Macrophage/Microglia-Induced Inflammation and Prevents Ischemic Brain Damage Via Binding to HMGB1.Journal of the American Heart Association · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High mobility group box 1 (HMGB1) is a ubiquitous nuclear protein that plays an important role in stabilizing nucleosomes and DNA repair. HMGB1 can be passively released from necrotic neurons or actively secreted by microglia, macrophages/monocytes, and neutrophils. Cerebral ischemia is a major cause of mortality and disability worldwide, and its outcome depends on the number of neurons dying due to hypoxia in the ischemic area. HMGB1 contributes to the pathogenesis of cerebral ischemia via mediating neuroinflammatory responses to cerebral ischemic injury. Extracellular HMGB1 regulates many neuroinflammatory events by interacting with its different cell surface receptors, such as receptors for advanced glycation end products, toll-like receptor (TLR)-2, and TLR-4. Additionally, HMGB1 can be redox-modified, thus exerting specific cellular functions in the ischemic brain and has different roles in the acute and late stages of cerebral ischemic injury. However, the role of HMGB1 in cerebral ischemia is complex and remains unclear. Herein, we summarize and review the research on HMGB1 in cerebral ischemia, focusing especially on the role of HMGB1 in hypoxic ischemia in the immature brain and in white matter ischemic injury. We also outline the possible mechanisms of HMGB1 in cerebral ischemia and the main strategies to inhibit HMGB1 pertaining to its potential as a novel critical molecular target in cerebral ischemic injury.
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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.