ArticleFrontiers in cellular neuroscience2019
High-Mobility Group Box 1 Contributes to Cerebral Cortex Injury in a Neonatal Hypoxic-Ischemic Rat Model by Regulating the Phenotypic Polarization of Microglia.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Systemic Inflammation and Central Neuronal Damage: The Relationship Between Neutrophil-to-Lymphocyte Ratio and Neuron-Specific Enolase in Acute Ischemic Stroke.Immunity, inflammation and disease · 2026Article
- Early HMGB1 Inhibition Reduces Hippocampal Injury During Adolescence in a Young Mouse Model of Radiation-Induced Brain Injury.Cellular and molecular neurobiology · 2026Article
- The umbilical cord blood exosome MFG-E8 alleviates hypoxic-ischemic encephalopathy brain injury in neonatal rats by restoring autophagy flux and inhibiting ferroptosis through GSK3β/β-catenin signaling.Regenerative therapy · 2025Article
- Inhibition of the HMGB1-RAGE Axis Attenuates Microglial Inflammation and Ameliorates Hypoxia-Induced Cognitive Impairment.International journal of molecular sciences · 2025Article
- Oseltamivir Phosphate Modulates CD24-Siglec-G/10 Interaction to Suppress Microglial-Driven Neuroinflammation After Cardiac Arrest.CNS neuroscience & therapeutics · 2025Article
- HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation.Translational stroke research · 2025Review
- Glycyrrhizin Attenuates White Matter Injury by Inhibiting Neuroinflammation through the HMGB1/TLR4 Pathway.Molecular neurobiology · 2025Article
- Neuroprotective Potential of Glycyrrhizic Acid in Ischemic Stroke: Mechanisms and Therapeutic Prospects.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Circulating HMGB1 in acute ischemic stroke and its association with post-stroke cognitive impairment.PeerJ · 2024Article
- Role of glia and extracellular matrix in controlling neuroplasticity in the central nervous system.Seminars in immunopathology · 2023Review
- High Mobility Group Box 1 (HMGB1): Potential Target in Sepsis-Associated Encephalopathy.Cells · 2023Review
- Ferroptosis: A Promising Therapeutic Target for Neonatal Hypoxic-Ischemic Brain Injury.International journal of molecular sciences · 2022Review
- Haptoglobin Regulates Macrophage/Microglia-Induced Inflammation and Prevents Ischemic Brain Damage Via Binding to HMGB1.Journal of the American Heart Association · 2022Article
- Article
- Glycyrrhizin Attenuates Hypoxic-Ischemic Brain Damage by Inhibiting Ferroptosis and Neuroinflammation in Neonatal Rats via the HMGB1/GPX4 Pathway.Oxidative medicine and cellular longevity · 2022Article
- Shaoyao-Gancao Decoction Promoted Microglia M2 Polarization via the IL-13-Mediated JAK2/STAT6 Pathway to Alleviate Cerebral Ischemia-Reperfusion Injury.Mediators of inflammation · 2022Article
- High-mobility Group Box 1 Contributes to Hypoxic-Ischemic Brain Damage by Facilitating Imbalance of Microglial Polarization through RAGE-PI3K/Akt Pathway in Neonatal Rats.International journal of medical sciences · 2022Article
- Long non-coding RNA LOC366613 alleviates the cerebral ischemic injury via regulating the miR-532-5p/phosphatase and tensin homolog axis.Bioengineered · 2021Article
- High mobility group box-1 protein as a therapeutic target in perinatal hypoxic-ischemic brain injury.Neural regeneration research · 2021Article
- Transient Global Ischemia-Induced Brain Inflammatory Cascades Attenuated by Targeted Temperature Management.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neonatal hypoxic-ischemic (HI) encephalopathy is a severe disease for which there is currently no curative treatment. Recent evidence suggests that high-mobility group box 1 (HMGB1) protein can promote neuroinflammation after stroke in adult rodents, but its role in perinatal hypoxic-ischemic brain damage (HIBD) remains largely uninvestigated. In the present work, the potential role of HMGB1 in the pathogenesis of HIBD was explored. A HIBD model was established in postpartum day 7 rat pups. HMGB1 expression, the cellular distribution of HMGB1, and microglial activation were all evaluated. Glycyrrhizin (GL), an inhibitor of HMGB1, was used to investigate whether the inhibition of HMGB1 modulated microglial M1/M2 polarization or attenuated brain damage after HI. HAPI microglial cells and primary neurons were cultured
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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.