ArticleClinical and experimental medicine2025
The mechanism of S100A8/A9 heterodimer promoting atherosclerotic thrombosis.
Article in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Serum S100A8 as a potential biomarker for diagnosis of antiphospholipid syndrome and risk stratification among aPL carriers.Lupus science & medicine · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
S100A8/A9 heterodimer is an inflammatory mediator that promotes atherosclerotic thrombosis (AT) and can also be used as a biomarker of the disease. However, its origin and mechanism of action remain largely unknown. This study aimed to elucidate the role of S100A8/A9 heterodimer produced by endothelial cells stimulated by neutrophil extracellular traps (NETs) in AT. The effects of NETs on human umbilical vein endothelial cells (HUVECs) were studied in a co-culture system. We detected the reactive oxygen species (ROS) activity, pyroptosis and S100A8/A9 heterodimer production of HUVECs, as well as the NF-κB signaling pathway activation. The effects of S100A8/A9 heterodimer on platelet activation and underlying mechanisms were investigated in washed human platelets, and then validated in FeCl3-injured carotid thrombosis model in rats. NETs stimulated HUVECs were found to produce ROS, then activating the NF-κB signaling pathway, inducing pyroptosis and the production of S100A8/A9 heterodimer. Additionally, S100A8/A9 heterodimer was found to induce the activation of platelets through activation of epidermal growth factor receptor (EGFR) signaling pathway. Subsequently, S100A8/A9 heterodimer mediated platelet activation thus inducing thrombus formation via the EGFR/PI3K/AKT and EGFR/p38 MAPK axes in platelets. Our results suggest that S100A8/A9 heterodimer produced by endothelial cells stimulated by NETs induces platelet activation by regulating the EGFR/PI3K/AKT and EGFR/p38 MAPK axes, thus promoting thrombosis. Our data provide new insights into the pathogenesis and therapeutic targets for AT.
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