ArticleCell death & disease2024
S100A8/A9
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
61 citing papers in PubMed.
- Identification of novel sepsis-related neutrophil subsets and surface markers for clinical diagnosis and outcome.Virulence · 2026Article
- Exploring the mechanism of polymorphonuclear neutrophils against sepsis based on immune model.Annals of medicine · 2026Review
- Autophagy determines the fate of immune cells by regulating metabolic remodeling and PANoptosis (Review).International journal of molecular medicine · 2026Review
- Programmed cell death in inflammation: interactions and holistic perspective.Cellular & molecular immunology · 2026Review
- Restricted TCR Diversity and Expansion of CD177MedComm · 2026Article
- Ginsenoside Rb1 ameliorates endothelial dysfunction in sepsis: Targeting the RhoA/ROCK pathway to modulate mitochondrial homeostasis and inflammation.Journal of ginseng research · 2026Article
- PANoptosis and Immune Remodeling in the Tumor Microenvironment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Plasma alarmin S100A8/A9 serves as a potential biomarker of major adverse cardiovascular events after acute myocardial infarction.Cardiovascular diagnosis and therapy · 2026Article
- GPR84 aggravates lung inflammation through activating ZBP1-PANoptosome mediated PANoptosis following IAV infection.Cell death discovery · 2026Article
- A neutrophil-intrinsic CKLF1-PKM2 axis drives glycolytic flux for de novo DAG synthesis and pro-inflammatory ROS production.Cell death and differentiation · 2026Article
- Neutrophil Heterogeneity: Molecules to Cellular Behavior.Life (Basel, Switzerland) · 2026Review
- Immune molecular mechanisms of PANoptosis in sepsis-induced acute kidney injury.Inflammation and regeneration · 2026Review
- Animal models of critical illness in the Asia-Pacific region: current practices, shared challenges, and future directions.Intensive care medicine experimental · 2026Review
- Thromboxane receptor activation in dendritic cells mitigates sepsis by suppressing S100a8/a9-mediated neutrophil recruitment.Signal transduction and targeted therapy · 2026Article
- S100A8 aggravates sepsis-associated encephalopathy by promoting PFKFB3-dependent glycolysis and microglial neuroinflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Targeting PANoptosis in atherosclerosis: bridging cell death mechanisms and therapy.Apoptosis : an international journal on programmed cell death · 2026Review
- Mitochondrial dysfunction in sepsis-induced immunoparalysis: from immune-cell metabolic reprogramming to clinical biomarkers.Frontiers in immunology · 2026Review
- PANoptosis in diabetic retinopathy: immunological insights into mechanisms and translational therapies.Frontiers in immunology · 2026Review
- Mitochondrial metabolic dysfunction drives PANoptosis in retinal pigment epithelium during fungal endophthalmitis: emerging roles of the MITF-FBXW7 axis.Frontiers in immunology · 2026Review
- Linking Metabolic and Mitochondrial Stress to Regulated Cell Death and Inflammatory Organ Injury in Sepsis.Journal of inflammation research · 2026Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100a8/a9, largely released by polymorphonuclear neutrophils (PMNs), belongs to the S100 family of calcium-binding proteins and plays a role in a variety of inflammatory diseases. Although S100a8/a9 has been reported to trigger endothelial cell apoptosis, the mechanisms of S100a8/a9-induced endothelial dysfunction during sepsis require in-depth research. We demonstrate that high expression levels of S100a8/a9 suppress Ndufa3 expression in mitochondrial complex I via downregulation of Nrf1 expression. Mitochondrial complex I deficiency contributes to NAD
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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.