ArticleInternational journal of molecular sciences2023
Deficiency of S100A9 Alleviates Sepsis-Induced Acute Liver Injury through Regulating AKT-AMPK-Dependent Mitochondrial Energy Metabolism.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed.
- Targeted activation of PPARG or AKT1 alleviates liver injury in mice with type 2 diabetes and sepsis by modulating inflammatory and metabolic pathways.Annals of medicine · 2026Article
- 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
- Review
- Predictive value of serum S100A8/A9 for liver dysfunction in pregnant women with chronic hepatitis B.Virology journal · 2026Article
- PAFAH2 deficiency drives sepsis-induced vascular leakage by promoting ECHS1-mediated suppression of protein crotonylation and mitochondrial dysfunction.Inflammation and regeneration · 2026Article
- Acteoside prevents high-fat diet-induced obesity by regulating brown adipose tissue production, lipid metabolism, and the gut microbiota.European journal of medical research · 2026Article
- Brusatol ameliorates psoriatic dyslipidemia by targeting IL-1β to restore AMPK-mediated lipid homeostasis.Chinese medicine · 2026Article
- MAGL-18c attenuates LPS-induced sepsis-associated liver injury by inhibiting TGF-β/Smad signaling and remodeling medium- and long-chain fatty acid metabolism.Frontiers in immunology · 2026Article
- Mitochondria-immunometabolism in sepsis-induced liver injury: mechanisms, biomarkers, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2026Review
- The S100A8/A9-NETosis feedback loop in sepsis: potential mechanisms, immune crosstalk, and therapeutic targeting.Frontiers in immunology · 2026Review
- Sirtuin 4 Knockout Aggravates Sepsis-Induced Acute Liver Injury by Enhancing Mitochondrial Fission and Mitophagy in Hepatocytes.Mediators of inflammation · 2026Article
- Gentisic acid ameliorates lumbar disc herniation by regulating M1/M2 Polarization via the MAPK14/S100A9/Rac1/2 pathway.Cell biology and toxicology · 2025Article
- Lipoxin A4 alleviates sepsis-induced acute liver injury by inhibiting inflammatory response and iron overload via JAK2/STAT3 signaling.Scientific reports · 2025Article
- Mitochondrial dysfunction in sepsis-induced liver injury: from pathophysiology to preclinical therapeutic targets.Journal of translational medicine · 2025Review
- Integrated Transcriptomic Analysis of S100A8/A9 as a Key Biomarker and Therapeutic Target in Sepsis Pathogenesis and AI Drug Repurposing.International journal of molecular sciences · 2025Article
- Identification and validation of key genes related to apoptosis in multiple organ dysfunction syndrome.European journal of medical research · 2025Article
- Neutrophil-Endothelium Interaction Mediated by S100A9 Promotes Pulmonary Vascular Remodeling During Pulmonary Hypertension.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Elevated levels of S100A8 and S100A9 exacerbate muscle mitochondrial fragmentation in sepsis-induced muscle atrophy.Communications biology · 2025Article
- TARGETING S100A9-TLR2 AXIS CONTROLS MACROPHAGE NLRP3 INFLAMMASOME ACTIVATION IN FATTY LIVER ISCHEMIA REPERFUSION INJURY.Shock (Augusta, Ga.) · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
Abstract
Acute liver injury (ALI) is recognized as a serious complication of sepsis in patients in intensive care units (ICUs). S100A8/A9 is known to promote inflammation and immune responses. However, the role of S100A8/A9 in the regulation of sepsis-induced ALI remains known. Our results indicated that S100A8/A9 expression was significantly upregulated in the livers of septic mice 24 h after cecal ligation and a puncture (CLP) operation. Moreover, S100A9-KO in mice markedly attenuated CLP-induced liver dysfunction and injury, promoting the AMPK/ACC/GLUT4-mediated increases in fatty acid and glucose uptake as well as the improvement in mitochondrial function and ATP production. In contrast, treatment with the AMPK inhibitor Compound C reversed the inhibitory effects of S100A9 KO on CLP-induced liver dysfunction and injury in vivo. Finally, the administration of the S100A9 inhibitor Paquinimod (Paq) to WT mice protected against CLP-induced mortality, liver injury and mitochondrial dysfunction. In summary, our findings demonstrate for the first time that S100A9 plays an important pro-inflammatory role in sepsis-mediated ALI by regulating AKT-AMPK-dependent mitochondrial energy metabolism and highlights that targeting S100A9 may be a promising new approach for the prevention and treatment of sepsis-related liver injury.
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What Socratic holds
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 Socratic graph.