ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2011
HMBG1 mediates ischemia-reperfusion injury by TRIF-adaptor independent Toll-like receptor 4 signaling.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 145 citations in OpenAlex.
- CD36-mediated hematoma absorption following intracerebral hemorrhage: negative regulation by TLR4 signaling.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Gut microbiota-dependent protection by Lactobacillus reuteri against renal injury in brain-dead rats.Scientific reports · 2026Article
- Microglial immunosurveillance after ischemic stroke: dynamic phenotypes, neurovascular interactions, and therapeutic opportunities.Frontiers in immunology · 2026Review
- M2 macrophage-secreted exosomal miR-216a regulates microglial polarization by targeting the HMGB1/TLR4/NF-κB pathway to alleviate bone cancer pain.American journal of translational research · 2026Article
- Acupuncture in Cerebral Ischemia-Reperfusion Injury: A Mechanistic Narrative Review of Innate Immune Sensing and Regulated Cell Death-Related Inflammatory Amplification.International journal of general medicine · 2026Review
- Therapeutic spectrum of Piperine in ischemic stroke: a literature review.Molecular biology reports · 2025Review
- HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation.Translational stroke research · 2025Review
- Article
- Targeting brain-peripheral immune responses for secondary brain injury after ischemic and hemorrhagic stroke.Journal of neuroinflammation · 2024Review
- RAGE plays key role in diabetic retinopathy: a review.Biomedical engineering online · 2023Review
- Monocyte-related cytokines/chemokines in cerebral ischemic stroke.CNS neuroscience & therapeutics · 2023Review
- HMGB1, angel or devil, in ischemic stroke.Brain and behavior · 2023Review
- Role of alarmins in poststroke inflammation and neuronal repair.Seminars in immunopathology · 2023Review
- Emerging diagnostic markers and therapeutic targets in post-stroke hemorrhagic transformation and brain edema.Frontiers in molecular neuroscience · 2023Review
- Overexpressed Toll-Like Receptor 2 and the Influence on the Severity of Acute Ischemic Stroke.Archives of Razi Institute · 2022Article
- Effects of butyphthalide on microglia polarization after intracerebral hemorrhage and the underlying mechanisms.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- TLR4 aggravates microglial pyroptosis by promoting DDX3X-mediated NLRP3 inflammasome activation via JAK2/STAT1 pathway after spinal cord injury.Clinical and translational medicine · 2022Article
- Role of DAMPs and of Leukocytes Infiltration in Ischemic Stroke: Insights from Animal Models and Translation to the Human Disease.Cellular and molecular neurobiology · 2022Review
- The Cellular Senescence Factor Extracellular HMGB1 Directly Inhibits Oligodendrocyte Progenitor Cell Differentiation and Impairs CNS Remyelination.Frontiers in cellular neuroscience · 2022Article
- Journey to a Receptor for Advanced Glycation End Products Connection in Severe Acute Respiratory Syndrome Coronavirus 2 Infection: With Stops Along the Way in the Lung, Heart, Blood Vessels, and Adipose Tissue.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
25 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-mobility group protein box-1 (HMGB1) has recently been recognized as a novel candidate in a specific upstream pathway promoting inflammation after brain ischemia. However, its downstream pathway and underlying mechanism have yet to be elucidated. The HMGB1 level in the acute cerebral infarct (ACI) group was significantly increased compared with that of control group, and correlated with the severity of neurologic impairment of ACI patients. Further, recombinant human HMGB1 (rhHMGB1) had no effect on microglia derived from mice lacking the Toll-like receptor 4 (TLR4(-/-)). Intracerebroventricular injection of rhHMGB1 in TLR4(+/+) mice cause significantly more injury after cerebral ischemia-reperfusion than control group. But, TLR4(-/-) mice administered with rhHMGB1 showed moderate impairment after ischemia-reperfusion than TLR4(+/+) mice. To determine the potential downstream signaling of HMGB1/TLR4 in cerebral ischemic injury, we used the ischemic-reperfusion model with Toll/interleukin-1 receptor domain-containing adaptor-inducing interferon-β knockout mice (TRIF(-/-)) and evaluated the activity and expression of TRIF pathway-related kinases. The results suggest that the TRIF pathway is not likely to be involved in TLR4-mediated ischemia brain injury. Finally, we found that TLR4 expressed by immigrant macrophages was involved in the development of ischemic brain damage. These results suggest that HMBG1 mediates ischemia-reperfusion injury by TRIF-adaptor independent Toll-like receptor 4 signaling. The TLR4 expressed by immigrant macrophages may be involved in the development of ischemic brain damage.
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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.