High-Mobility Group Box-1 and Its Potential Role in Perioperative Neurocognitive Disorders

Saxena, Sarah; Kruys, Véronique; Jongh, R. De; Vamecq, Jòseph; Maze, Mervyn

doi:10.3390/cells10102582

Cited by 10 publications

(10 citation statements)

References 116 publications

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“…HMGB1 shuttles from the nucleus to the cytoplasm via NLS acetylation, phosphorylation, or methylation, and can both passively (via damaged and/or necrotic cells) and actively (via activated monocytes/macrophages) release into extracellular space and circulation. The biological functions of HMGB1 are dependent on its location: (1) nuclear HMGB1 is involved in several nuclear processes, such as chromatin stabilization, replication, DNA-damage repair and gene transcription; (2) cytoplasmic HMGB1 participates in the regulation of AIM2 (absent in melanoma 2) inflammasome, autophagy, and mitophagy; and (3) extracellular HMGB1 (eHMGB1) functions as a proinflammatory mediator [ 19 , 20 ]. The translocation of HMGB1 between cellular compartments is a dynamic process triggered by variety of cell stresses and diseases (sepsis, trauma, hemorrhagic shock, ischemia, etc.)…”

Section: Introductionmentioning

confidence: 99%

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HMGB1 Inhibition to Ameliorate Organ Failure and Increase Survival in Trauma

et al. 2022

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Several preclinical and clinical reports have demonstrated that levels of circulating high mobility group box 1 protein (HMGB1) are increased early after trauma and are associated with systemic inflammation and clinical outcomes. However, the mechanisms of the interaction between HMGB1 and inflammatory mediators that lead to the development of remote organ damage after trauma remain obscure. HMGB1 and inflammatory mediators were analyzed in plasma from 54 combat casualties, collected on admission to a military hospital in Iraq, and at 8 and 24 h after admission. In total, 45 (83%) of these patients had traumatic brain injury (TBI). Nine healthy volunteers were enrolled as controls. HMGB1 plasma levels were significantly increased in the first 8 h after admission, and were found to be associated with systemic inflammatory responses, injury severity score, and presence of TBI. These data provided the rationale for designing experiments in rats subjected to blast injury and hemorrhage, to explore the effect of HMGB1 inhibition by CX-01 (2-O, 3-O desulfated heparin). Animals were cannulated, then recovered for 5–7 days before blast injury in a shock tube and volume-controlled hemorrhage. Blast injury and hemorrhage induced an early increase in HMGB1 plasma levels that coincided with severity of tissue damage and mortality. CX-01 inhibited systemic HMGB1 activity, decreased local and systemic inflammatory responses, significantly reduced tissue and organ damage, and tended to increase survival. These data suggest that CX-01 has potential as an adjuvant treatment for traumatic hemorrhage.

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Section: Introductionmentioning

confidence: 99%

“…The translocation of HMGB1 between cellular compartments is a dynamic process triggered by variety of cell stresses and diseases (sepsis, trauma, hemorrhagic shock, ischemia, etc.) [ 19 , 20 , 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

HMGB1 Inhibition to Ameliorate Organ Failure and Increase Survival in Trauma

et al. 2022

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“…The up-regulated protein level of HMGB1 was detected in hippocampus of rat brain following surgery and anesthesia [ 17 ]. HMGB1 acts as a damage-associated molecular pattern (DAMP) to bind to TLR and the receptor for advance glycosylation end product (RAGE) on circulating bone-marrow-derived monocytes (BM-DM) and endothelial cells, triggering the production of pro-inflammatory cytokines and facilitating leukocyte migration and immune cell recruitment, resulting in neuroinflammation and PND [ 40 , 41 ]. Therefore, neutralizing antibodies to HMGB1 may be a potential treatment for PND.…”

Section: Introductionmentioning

confidence: 99%

Targeting neuroinflammation as a preventive and therapeutic approach for perioperative neurocognitive disorders

Cheng

Wan

Cong

et al. 2022

J Neuroinflammation

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Perioperative neurocognitive disorders (PND) is a common postoperative complication associated with regional or general anesthesia and surgery. Growing evidence in both patient and animal models of PND suggested that neuroinflammation plays a critical role in the development and progression of this problem, therefore, mounting efforts have been made to develop novel therapeutic approaches for PND by targeting specific factors or steps alongside the neuroinflammation. Multiple studies have shown that perioperative anti-neuroinflammatory strategies via administering pharmacologic agents or performing nonpharmacologic approaches exert benefits in the prevention and management of PND, although more clinical evidence is urgently needed to testify or confirm these results. Furthermore, long-term effects and outcomes with respect to cognitive functions and side effects are needed to be observed. In this review, we discuss recent preclinical and clinical studies published within a decade as potential preventive and therapeutic approaches targeting neuroinflammation for PND.

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“…The neuroinflammatory hypothesis asserts that (1) surgical trauma causes local inflammation and peripheral pro-inflammatory cytokine cascades, (2) pro-inflammatory cytokines in turn cause BBB disruption and central nervous system (CNS) inflammation, which (3) results in functional and structural neuronal injury. We present a concise overview with preclinical and clinical data where appropriate; for more detailed reviews, please see ( Safavynia and Goldstein, 2018 ; Saxena and Maze, 2018 ; Saxena et al, 2021 ).…”

Section: Risk Factorsmentioning

confidence: 99%

Mitigation of perioperative neurocognitive disorders: A holistic approach

Safavynia

Goldstein

Evered

2022

Front. Aging Neurosci.

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William Morton introduced the world to ether anesthesia for use during surgery in the Bullfinch Building of the Massachusetts General Hospital on October 16, 1846. For nearly two centuries, the prevailing wisdom had been that the effects of general anesthetics were rapidly and fully reversible, with no apparent long-term adverse sequelae. Despite occasional concerns of a possible association between surgery and anesthesia with dementia since 1887 (Savage, 1887), our initial belief was robustly punctured following the publication in 1998 of the International Study of Post-Operative Cognitive Dysfunction [ISPOCD 1] study by Moller et al. (1998) in The Lancet, in which they demonstrated in a prospective fashion that there were in fact persistent adverse effects on neurocognitive function up to 3 months following surgery and that these effects were common. Since the publication of that landmark study, significant strides have been made in redefining the terminology describing cognitive dysfunction, identifying those patients most at risk, and establishing the underlying etiology of the condition, particularly with respect to the relative contributions of anesthesia and surgery. In 2018, the International Nomenclature Consensus Working Group proposed new nomenclature to standardize identification of and classify perioperative cognitive changes under the umbrella of perioperative neurocognitive disorders (PND) (Evered et al., 2018a). Since then, the new nomenclature has tried to describe post-surgical cognitive derangements within a unifying framework and has brought to light the need to standardize methodology in clinical studies and motivate such studies with hypotheses of PND pathogenesis. In this narrative review, we highlight the relevant literature regarding recent key developments in PND identification and management throughout the perioperative period. We provide an overview of the new nomenclature and its implications for interpreting risk factors identified by clinical association studies. We then describe current hypotheses for PND development, using data from clinical association studies and neurophysiologic data where appropriate. Finally, we offer broad clinical guidelines for mitigating PND in the perioperative period, highlighting the role of Brain Enhanced Recovery After Surgery (Brain-ERAS) protocols.

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High-Mobility Group Box-1 and Its Potential Role in Perioperative Neurocognitive Disorders

Cited by 10 publications

References 116 publications

HMGB1 Inhibition to Ameliorate Organ Failure and Increase Survival in Trauma

HMGB1 Inhibition to Ameliorate Organ Failure and Increase Survival in Trauma

Targeting neuroinflammation as a preventive and therapeutic approach for perioperative neurocognitive disorders

Mitigation of perioperative neurocognitive disorders: A holistic approach

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