ArticleScientific reports2023
Acute muscle mass loss was alleviated with HMGB1 neutralizing antibody treatment in severe burned rats.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Mitochondria as a Therapeutic Target for Burn Injury.Biomolecules · 2026Review
- Enhanced Burn Wound Healing and Conversion Prevention Through Inhibition of High Mobility Group Box 1 in a Scald Burn Rat Model.Journal of burn care & research : official publication of the American Burn Association · 2026Article
- Immediate post-injury HMGB1 neutralization prevents synaptic dysfunction in burn and hindlimb unloaded rats.Frontiers in immunology · 2026Article
- Unveiling the molecular mechanisms of burn injury through integrated single-cell and bulk transcriptomic analysis.PloS one · 2026Article
- Evaluating skeletal muscle wasting and weakness in models of critical illness.Clinical science (London, England : 1979) · 2025Review
- The immunoglobulin of yolk and cerium oxide-based fibrous poly(L-lactide-co-glycolide)/gelatin dressings enable skin regeneration in an infectious wound model.Materials today. Bio · 2025Article
- Mild burn amplifies the locomotive depression in demyelinated mice without muscle pathophysiological changes.PloS one · 2024Article
- Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Burn injury is associated with muscle wasting, though the involved signaling mechanisms are not well understood. In this study, we aimed to examine the role of high mobility group box 1 (HMGB1) in signaling hyper-inflammation and consequent skeletal muscle impairment after burn. Sprague Dawley rats were randomly assigned into three groups: (1) sham burn, (2) burn, (3) burn/treatment. Animals in group 2 and group 3 received scald burn on 30% of total body surface area (TBSA) and immediately treated with chicken IgY and anti-HMGB1 antibody, respectively. Muscle tissues and other samples were collected at 3-days after burn. Body mass and wet/dry weights of the hind limb muscles (total and individually) were substantially decreased in burn rats. Acute burn provoked the mitochondrial stress and cell death and enhanced the protein ubiquitination and LC3A/B levels that are involved in protein degradation in muscle tissues. Further, an increase in muscle inflammatory infiltrate associated with increased differentiation, maturation and proinflammatory activation of bone marrow myeloid cells and αβ CD4
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