ArticleFrontiers in pharmacology2023
Blockage of S100A8/A9 ameliorates septic nephropathy in mice.
Article in Frontiers in pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Restricted TCR Diversity and Expansion of CD177MedComm · 2026Article
- The Role of S100A8/A9 in Autoimmune Eye Diseases: From Pathogenesis to Targeted Therapy.Investigative ophthalmology & visual science · 2026Review
- Genome-wide DNA methylation analysis revealed epigenetic mechanism underlying end-stage renal disease.Nature communications · 2026Article
- Proteomic signatures of renal recovery from acute kidney injury-a translational study in critically ill postoperative patients.Intensive care medicine experimental · 2026Article
- Exploring the mechanism of endothelial Pim-1 upregulation of tissue factor to initiate the hypercoagulable state in sepsis.Molecular medicine (Cambridge, Mass.) · 2026Article
- Elucidating the therapeutic efficacy and mechanisms of arctigenin in ameliorating renal fibrosis: a combined transcriptomic and proteomic study.Frontiers in pharmacology · 2026Article
- The S100A8/A9-NETosis feedback loop in sepsis: potential mechanisms, immune crosstalk, and therapeutic targeting.Frontiers in immunology · 2026Review
- S100A8/A9 in Kidney Diseases: Mechanisms, Spatiotemporal Regulation, Biomarker Potential, and Therapeutic Implications.Journal of inflammation research · 2026Review
- Identification and validation of key genes related to apoptosis in multiple organ dysfunction syndrome.European journal of medical research · 2025Article
- Critical Role of S100A9 in Sepsis-associated Acute Kidney Injury: Mechanistic Insights through Pyroptosis Pathway Modulation.Inflammation · 2025Article
- Elevated levels of S100A8 and S100A9 exacerbate muscle mitochondrial fragmentation in sepsis-induced muscle atrophy.Communications biology · 2025Article
- Single-cell RNA sequencing reveals that myeloid S100A8/A9 is a novel regulator of the transition from adaptive hypertrophy to heart failure after pressure overload.Theranostics · 2025Article
- S100A8/S100A9 through PAD4 activation of neutrophil extracellular traps promotes granulomatous lobular mastitis.Frontiers in immunology · 2025Article
- The immunosuppressive mechanisms induced by sepsis and the corresponding treatment strategies.Frontiers in immunology · 2025Review
- Research progress on damage-associated molecular patterns in acute kidney injury.Frontiers in immunology · 2025Review
- Blood calprotectin as a biomarker for infection and sepsis - the prospective CASCADE trial.BMC infectious diseases · 2024Observational
- Blocking S100A9-signaling is detrimental to the initiation of anti-tumor immunity.Frontiers in immunology · 2024Article
- Integrated multi-omics and artificial intelligence to explore new neutrophils clusters and potential biomarkers in sepsis with experimental validation.Frontiers in immunology · 2024Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Septic acute kidney injury (AKI) is the commonest cause of complication of sepsis in intensive care units, but its pathophysiology remains unclear. Calprotectin (S100A8/A9), which is a damage-associated molecular patterns (DAMPs) molecule, exerts a critical role in modulating leukocyte recruitment and inflammatory response during various diseases. However, role of S100A8/A9 in septic AKI is largely unknown. In this research, Septic AKI was triggered by cecal ligation and puncture (CLP) operation in wild-type mice, which treated with or without an S100A9 inhibitor, Paquinimod (Paq, 10 mg/kg) that prevents S100A8/A9 to bind to Toll-like receptor 4 (TLR4). Renal function, pathological changes, cell death, and oxidative stress were evaluated. Our research indicated that the mRNA and protein expression of S100A9 are time-dependently elevated in the kidney following CLP. Moreover, the administration of Paq for 24 h significantly improved CLP-induced renal dysfunction and pathological alterations compared with vehicle treatment in mice. These beneficial effects were associated with the inhibition of CLP-triggered renal tubular epithelial cell apoptosis, inflammation, superoxide production, and mitochondrial dynamic imbalance. What's more, we further confirmed the above findings by cell co-culture experiments. Our study demonstrates that S100A9 is a prominent protein to lead to septic AKI, and the selective inhibition of S100A9 could represent a new therapeutic approach which can treat septic AKI.
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