ArticleCells2022
HMGB1 Promotes In Vitro and In Vivo Skeletal Muscle Atrophy through an IL-18-Dependent Mechanism.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- ITCH-Mediated Ubiquitination and Degradation of THBS1: A Key Mechanism for Enhancing Mitochondrial Biogenesis and Alleviating Mouse Skeletal Muscle Atrophy.Acta physiologica (Oxford, England) · 2026Article
- IL-18 Binding Protein, a biomarker of strength maintenance after surgery but reduced physical performance in age-related sarcopenia.PloS one · 2026Article
- Mechanism of Hypoxia-Induced HMGB1 Regulating NLRP3 Inflammasome/Caspase-1 Pathway-Mediated Pyroptosis in Myocardial Ischemia Reperfusion Injury Through the Nrf2/HO-1 Pathway.CNS neuroscience & therapeutics · 2025Article
- Immuno-metabolic diseases and therapeutics: molecular mechanisms via inflammasome signaling.Cell communication and signaling : CCS · 2025Review
- Sustained Accumulation of Molecular Clock Suppressors Period 1 and Period 2 Promotes C2C12 Myotube Atrophy Through an Autocrine-Mediated Mechanism With Relevance to Androgen Deprivation-Induced Limb Muscle Mass Loss.Function (Oxford, England) · 2025Article
- Caprylic Acid Restores Branched-Chain Amino Acid Metabolism in a Mouse Cachexia Model.Current issues in molecular biology · 2025Article
- Cell-cell fusion: To lose one life and begin another.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Antcin K ameliorates cardiotoxin-induced skeletal muscle injury and inflammation via IL-10 regulation.International journal of biological sciences · 2025Article
- Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024Review
- A global view of altered ligand-receptor interactions in bone marrow aging based on single-cell sequencing.Computational and structural biotechnology journal · 2024Article
- Article
- Inflammation balance in skeletal muscle damage and repair.Frontiers in immunology · 2023Review
- Melatonin improves muscle injury and differentiation by increasing Pax7 expression.International journal of biological sciences · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle atrophy occurs due to muscle wasting or reductions in protein associated with aging, injury, and inflammatory processes. High-mobility group box-1 (HMGB1) protein is passively released from necrotic cells and actively secreted by inflammatory cells, and is implicated in the pathogenesis of various inflammatory and immune diseases. HMGB1 is upregulated in muscle inflammation, and circulating levels of the proinflammatory cytokine interleukin-18 (IL-18) are upregulated in patients with sarcopenia, a muscle-wasting disease. We examined whether an association exists between HMGB1 and IL-18 signaling in skeletal muscle atrophy. HMGB1-induced increases of IL-18 levels enhanced the expression of muscle atrophy markers and inhibited myogenic marker expression in C2C12 and G7 myoblast cell lines. HMGB1-induced increases of IL-18 production in C2C12 cells involved the RAGE/p85/Akt/mTOR/c-Jun signaling pathway. HMGB1 short hairpin RNA (shRNA) treatment rescued the expression of muscle-specific differentiation markers in murine C2C12 myotubes and in mice with glycerol-induced muscle atrophy. HMGB1 and IL-18 signaling was suppressed in the mice after HMGB1 shRNA treatment. These findings suggest that the HMGB1/IL-18 axis is worth targeting for the treatment of skeletal muscle atrophy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.