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Ankarcrona, M., Dypbukt, J.M. and Bonfoco, E., et al. (1995) Glutamate-Induced Neuronal Death: A Succession of Necrosis or Apoptosis Depending on Mitochondrial Function. Neuron, 15, 961-973.
https://doi.org/10.1016/0896-6273(95)90186-8

has been cited by the following article:

  • TITLE: High Mobility Group Box 1 and Traumatic Brain Injury

    AUTHORS: Seidu A. Richard, Wu Min, Zhaoliang Su, Huaxi Xu

    KEYWORDS: HMGB1, TBI, Biomarker, Brain Edema, Coagulation, Anti-HMGB1 Therapy

    JOURNAL NAME: Journal of Behavioral and Brain Science, Vol.7 No.2, February 9, 2017

    ABSTRACT: Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. We identify High Mobility Group Box 1 (HMGB1) as a novel causative factor in the development of cerebral oedema, mediating coagulation, preventing secondary brain damage as well as serving as a novel therapeutic target to limit secondary neurological injury after TBI. As a prototypical danger associated molecular patterns (DAMP), HMGB1 is released from necrotic neurons via a NR2B-mediated mechanism during TBI. The secretion of HMGB1 requires severe injury and tissue hypoperfusion, and is associated with posttraumatic coagulation abnormalities, activation of complement and severe systemic inflammatory response. HMGB1 is clinically associated with elevated intracranial pressure (ICP) in patients and functionally promoted cerebral edema after TBI. The detrimental effects of HMGB1 is mediated at least in part between activation of microglial toll-like receptor 4 (TLR4) and the subsequent expression of the astrocytic water channel aquaporin-4 (AQP4). Anti-HMGB1mAb remarkably inhibited fluid percussion-induced brain edema by inhibiting HMGB1 translocation, protection of blood-brain barrier (BBB) integrity, suppression of inflammatory molecule expression and improvement of motor function. Our review demonstrates the pathological role of HMGB1 as well as the possible therapeutic valve of HMGB1 in patients with TBI.