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Related Experiment Video

Updated: Jul 1, 2026

Reliable Isolation of Central Nervous System Microvessels Across Five Vertebrate Groups
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High Mobility Group Box 1 (HMGB1): Potential Target in Sepsis-Associated Encephalopathy.

Bram DeWulf1, Laurens Minsart2, Franck Verdonk3

  • 1Department of Anesthesia-Critical Care, AZ Sint-Jan Brugge Oostende AV, 8000 Bruges, Belgium.

Cells
|April 13, 2023
PubMed
Summary
This summary is machine-generated.

Sepsis-associated encephalopathy (SAE) lacks diagnostic tools. Targeting high mobility group box 1 (HMGB1) may mitigate neuroinflammation and complement current sepsis-induced encephalopathy treatments.

Keywords:
HMGB1high mobility group box 1sepsissepsis-associated encephalopathy

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Area of Science:

  • Critical Care Medicine
  • Neuroscience
  • Immunology

Background:

  • Sepsis-associated encephalopathy (SAE) presents diagnostic and definition challenges for intensivists.
  • Risk factors include age, genetics, and pre-existing neuropsychiatric conditions, with certain infections posing higher risks.
  • Current intensive care unit (ICU) management relies on non-pharmacological support.

Purpose of the Study:

  • To review the role of high mobility group box 1 (HMGB1) in SAE pathogenesis.
  • To explore HMGB1-targeted strategies for mitigating sepsis-induced neuroinflammation.
  • To discuss HMGB1 as a potential therapeutic target for SAE.

Main Methods:

  • Review of pre-clinical studies on HMGB1 in sepsis and neurological disorders.
  • Analysis of HMGB1's role in neuroinflammation and blood-brain barrier disruption.
  • Examination of inflammatory cascades involving HMGB1.

Main Results:

  • HMGB1, an alarmin, is implicated in the pathogenesis of SAE.
  • Extracellular HMGB1 translocation triggers neuroinflammatory reactions and compromises the blood-brain barrier.
  • Targeting HMGB1 may inhibit inflammatory cascades.

Conclusions:

  • HMGB1 plays a significant role in neuroinflammation following sepsis.
  • Inhibiting HMGB1-mediated inflammation offers a potential therapeutic strategy for SAE.
  • Targeting HMGB1 could complement existing non-pharmacological interventions for SAE.