ReviewAnnals of the New York Academy of Sciences2010
Biphasic actions of HMGB1 signaling in inflammation and recovery after stroke.
Review in Annals of the New York Academy of Sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
77 citing papers in PubMed, 139 citations in OpenAlex.
- HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation.Translational stroke research · 2025Review
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 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
- Coronary Microvascular Dysfunction is Associated with Augmented Lysosomal Signaling in Hypercholesterolemic Mice.bioRxiv : the preprint server for biology · 2024Article
- Circulating HMGB1 in acute ischemic stroke and its association with post-stroke cognitive impairment.PeerJ · 2024Article
- USP25 Inhibits Neuroinflammatory Responses After Cerebral Ischemic Stroke by Deubiquitinating TAB2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Neuroinflammatory Biomarkers in the Brain, Cerebrospinal Fluid, and Blood After Ischemic Stroke.Molecular neurobiology · 2023Review
- miR-590-3p protects against ischaemia/reperfusion injury in an oxygen-glucose deprivation and reoxygenation cellular model by regulating HMGB1/TLR4/MyD88/NF-κB signalling.Histology and histopathology · 2023Article
- Engeletin alleviates cerebral ischemia reperfusion-induced neuroinflammation via the HMGB1/TLR4/NF-κB network.Journal of cellular and molecular medicine · 2023Article
- Role of alarmins in poststroke inflammation and neuronal repair.Seminars in immunopathology · 2023Review
- Neuroimmune mechanisms and therapies mediating post-ischaemic brain injury and repair.Nature reviews. Neuroscience · 2023Review
- Modulation of α7nAchR by Melatonin Alleviates Ischemia and Reperfusion-Compromised Integrity of Blood-Brain Barrier Through Inhibiting HMGB1-Mediated Microglia Activation and CRTC1-Mediated Neuronal Loss.Cellular and molecular neurobiology · 2022Article
- Review: The role of HMGB1 in spinal cord injury.Frontiers in immunology · 2022Review
- Reduction of neuroinflammation alleviated mouse post bone fracture and stroke memory dysfunction.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Toll-Like Receptor Signaling Pathways: Novel Therapeutic Targets for Cerebrovascular Disorders.International journal of molecular sciences · 2021Review
- Review
- Gut Microbiota-Related Effects of Tanhuo Decoction in Acute Ischemic Stroke.Oxidative medicine and cellular longevity · 2021Article
- AKAP12 Supports Blood-Brain Barrier Integrity against Ischemic Stroke.International journal of molecular sciences · 2020Article
- Bone Fracture Enhanced Blood-Brain Barrier Breakdown in the Hippocampus and White Matter Damage of Stroke Mice.International journal of molecular sciences · 2020Article
- Microglia knockdown reduces inflammation and preserves cognition in diabetic animals after experimental stroke.Journal of neuroinflammation · 2020Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Stroke induces a complex web of pathophysiology that may evolve over hours to days and weeks after onset. It is now recognized that inflammation is an important phenomenon that can dramatically influence outcomes after stroke. In this minireview, we explore the hypothesis that inflammatory signals after stroke are biphasic in nature. The high-mobility group box 1 (HMGB1) protein is discussed as an example of this idea. HMGB1 is normally present in the nucleus. Under ischemic conditions, it is released extracellularly from many types of cells. During the acute phase poststroke, HMGB1 promotes necrosis and influx of damaging inflammatory cells. However, during the delayed phase poststroke, HMGB1 can mediate beneficial plasticity and recovery in many cells of the neurovascular unit. These emerging findings support the hypothesis that inflammation after stroke can be both detrimental and beneficial, depending on the cellular situations involved.
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What OpenQuestion holds
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.