ArticleCommunications biology2025
Elevated levels of S100A8 and S100A9 exacerbate muscle mitochondrial fragmentation in sepsis-induced muscle atrophy.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- S100A8/S100A9 released by CD11bExperimental & molecular medicine · 2026Article
- Lung microbiota-derived deoxyinosine alleviates TBI-aggravated sepsis-induced lung injury via the S100A9/RAGE pathway.Journal of neuroinflammation · 2026Article
- Calprotectin and Sarcopenia in COPD: Biomarker, Bystander or Target?Journal of cachexia, sarcopenia and muscle · 2026Article
- S100A9 as a shared biomarker and mediator of metabolic dysfunction in peripheral artery disease and sarcopenia.Frontiers in genetics · 2026Article
- Sarcopenia and sepsis fuel a self-perpetuating cycle of immunometabolism decline.Frontiers in immunology · 2026Review
- Adipose-Derived Extracellular Vesicles and Intercellular Crosstalk With Skeletal Muscle: Implications for Sarcopenic Obesity and Metabolic Dysregulation.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026Review
- Article
- RAGE contributes to persistent sepsis-induced muscle and mitochondrial alterations.Scientific reports · 2025Article
- Rethinking post-sepsis syndrome: linking cellular dysfunction to the clinical picture.Critical care (London, England) · 2025Review
- Identification of sepsis biomarkers through glutamine metabolism-mediated immune regulation: a comprehensive analysis employing mendelian randomization, multi-omics integration, and machine learning.Frontiers in immunology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Sepsis-induced skeletal muscle atrophy is common in septic patients with the increases risk of mortality and is associated with myocellular mitochondrial dysfunction. Nevertheless, the specific mechanism of sepsis muscle atrophy remains unclear. Here we conducted a clinical retrospective analysis and observed the elevation of skeletal muscle index (ΔSMI) was an independent risk factor for 60-day mortality in septic patients. Moreover, in mouse model of sepsis, the skeletal muscle atrophy was also observed, which was associated with the upregulation of S100a8/a9-mediated mitochondrial dysfunction. Inhibition of S100a8/a9 significantly improved mitochondrial function and alleviated muscle atrophy. Conversely, administration of recombinant S100a8/a9 protein exacerbated mitochondrial energy exhaustion and myocyte atrophy. Mechanistically, S100a8/a9 binding to RAGE induced Drp1 phosphorylation and mitochondrial fragmentation, resulting in muscle atrophy. Additionally, RAGE ablation or administration of Drp1 inhibitor significantly reduced Drp1-mediated mitochondrial fission, improved mitochondrial morphology and function. Our findings indicated the pivotal role of S100a8/a9 in driving the mitochondrial fragmentation in septic muscle atrophy. Targeting S100a8/a9-RAGE-initiated mitochondrial fission might offer a promising therapeutic intervention against septic muscle atrophy.
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