ReviewTranslational stroke research2025
HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation.
Review in Translational stroke research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed.
- Review
- Involvement of COX-2 in the Neurovascular Unit Damage Through Up-Regulating Calpain/PARP/NF-κB Inflammatory Signaling During Ischemic Stroke.Neurochemical research · 2026Article
- 1,8-Cineole Promotes the Proliferation of Neural Stem Cells and Inhibits Oxidative Damage Induced by Ischemic Stroke via the Wnt/β-Catenin Signaling Pathway.Molecular neurobiology · 2026Article
- Epigenetic Regulation of the NET Formation-Blood-Brain Barrier Axis in Ischemic Stroke: Mechanisms, Therapeutic Targets and Translational Perspectives.Neurology international · 2026Review
- Anti-HMGB1 Antibody Therapy Ameliorates Depression Following Spinal Cord Injury in Rats by Inhibiting Ferroptosis.Journal of cellular and molecular medicine · 2026Article
- Interference with HMGB1 Inhibits Neuronal Ferroptosis Following Spinal Cord Injury through Targeting ACSL4.Neurochemical research · 2026Article
- Pyroptosis in cerebral ischemia‑reperfusion injury: Molecular mechanisms and therapeutic implications (Review).Molecular medicine reports · 2026Review
- From insult to hyperexcitability: pharmacological targeting of MyD88 and JAK/STAT3 pathways in epilepsy.Inflammopharmacology · 2026Review
- Artemisinin attenuates 3-nitropropionic acid-induced neurodegeneration via HMGB1/TLR4/NF-κB modulation in a rat model of huntington's disease.Archives of pharmacal research · 2026Article
- Recent advances in stroke biomarkers - implications for prognosis and treatment.Current opinion in neurology · 2026Review
- Endothelial ferroptosis in blood-brain barrier dysfunction and neuroinflammation: mechanisms and immune-vascular crosstalk.Frontiers in immunology · 2026Review
- The hidden battlefield: platelet function in the wake of severe trauma.Frontiers in immunology · 2026Review
- Prognostic value of IL-6, HMGB1, and TLR4 in bronchoalveolar lavage fluid of patients with community-acquired pneumonia.American journal of translational research · 2026Article
- Baicalin-geniposide attenuates pulmonary inflammation and vascular injury via HMGB1 blockade: insights from a cerebral ischemia-reperfusion model and implications for pulmonary hypertension.Frontiers in pharmacology · 2026Article
- Review
- Tracing Inflammation in Ischemic Stroke: Biomarkers and Clinical Insight.International journal of molecular sciences · 2025Review
- Chemerin 15 enhances microglial phagocytosis to attenuate cerebral ischemia-reperfusion injury through the ChemR23/p38 MAPK pathway.iScience · 2025Article
- Microglial Autophagy and Mitophagy in Ischemic Stroke: From Dual Roles to Therapeutic Modulation.Biology · 2025Review
- Examining the Impact of Microglia on Ischemic Stroke With an Emphasis on the Metabolism of Immune Cells.CNS neuroscience & therapeutics · 2025Review
- Comprehensive transcriptomic analysis integrating bulk and single-cell RNA-seq with machine learning to identify and validate mitochondrial unfolded protein response biomarkers in patients with ischemic stroke.Frontiers in cell and developmental biology · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Stroke in China is distinguished by its high rates of morbidity, recurrence, disability, and mortality. The ultra-early administration of rtPA is essential for restoring perfusion in acute ischemic stroke, though it concurrently elevates the risk of hemorrhagic transformation. High-mobility group box 1 (HMGB1) emerges as a pivotal player in neuroinflammation after brain ischemia and ischemia-reperfusion. Released passively by necrotic cells and actively secreted, including direct secretion of HMGB1 into the extracellular space and packaging of HMGB1 into intracellular vesicles by immune cells, glial cells, platelets, and endothelial cells, HMGB1 represents a prototypical damage-associated molecular pattern (DAMP). It is intricately involved in the pathogenesis of atherosclerosis, thromboembolism, and detrimental inflammation during the early phases of ischemic stroke. Moreover, HMGB1 significantly contributes to neurovascular remodeling and functional recovery in later stages. Significantly, HMGB1 mediates hemorrhagic transformation by facilitating neuroinflammation, directly compromising the integrity of the blood-brain barrier, and enhancing MMP9 secretion through its interaction with rtPA. As a systemic inflammatory factor, HMGB1 is also implicated in post-stroke depression and an elevated risk of stroke-associated pneumonia. The role of HMGB1 extends to influencing the pathogenesis of ischemia by polarizing various subtypes of immune and glial cells. This includes mediating excitotoxicity due to excitatory amino acids, autophagy, MMP9 release, NET formation, and autocrine trophic pathways. Given its multifaceted role, HMGB1 is recognized as a crucial therapeutic target and prognostic marker for ischemic stroke and hemorrhagic transformation. In this review, we summarize the structure and redox properties, secretion and pathways, regulation of immune cell activity, the role of pathophysiological mechanisms in stroke, and hemorrhage transformation for HMGB1, which will pave the way for developing new neuroprotective drugs, reduction of post-stroke neuroinflammation, and expansion of thrombolysis time window.
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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.