ArticleEMBO reports2024
CMTM3 regulates neutrophil activation and aggravates sepsis through TLR4 signaling.
Article in EMBO reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Engineered hollow Prussian blue nanoparticles for synergistic anti-inflammatory therapy in sepsis.Materials today. Bio · 2026Article
- The Bioinformatics Analysis of Publicly Available Datasets and Validation in a Mouse Model of Myocardial Infarction Through Coronary Artery Ligation.Journal of inflammation research · 2026Article
- Emerging role of N-acetyltransferase 10 in diseases: RNA ac4C modification and beyond.Molecular biomedicine · 2025Review
- Association between neutrophil-platelet ratio and 28-day mortality in patients with sepsis: a retrospective analysis based on MIMIC-IV database.BMC infectious diseases · 2025Article
- The J-shaped association between the ratio of neutrophil counts to prognostic nutritional index and mortality in ICU patients with sepsis: a retrospective study based on the MIMIC database.Frontiers in cellular and infection microbiology · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
Regulation of neutrophil activation plays a significant role in managing sepsis. CKLF-like MARVEL transmembrane domain containing (CMTM)3 is a membrane protein involved in immune response. Here, we find that CMTM3 expression is elevated in sepsis and plays a crucial role in mediating the imbalance of neutrophil migration. Cmtm3 knockout improves the survival rate of septic mice, mitigate inflammatory responses, and ameliorate organ damage. Mechanistically, the deletion of Cmtm3 reduced the expression of Toll-like receptor 4 (TLR4) on neutrophils, leading to a decrease in the expression of C-X-C motif chemokine receptor 2 (CXCR2) on the cell membrane. This resulted in a reduced migration of neutrophils from the bone marrow to the bloodstream, thereby attenuating their recruitment to vital organs. Our findings suggest that targeting CMTM3 holds promise as a therapeutic approach to ameliorate the dysregulation of neutrophil migration and multi-organ damage associated with sepsis.
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Registered trials
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