ArticleFrontiers in immunology2026
Knockout of p47phox inhibits deep vein thrombosis by regulating the PAC-1/FNG/MAC-1 signaling axis and ameliorating mitochondrial dysfunction.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: To elucidate the role and molecular mechanism of the NADPH oxidase key subunit p47phox in deep vein thrombosis (DVT) formation by investigating its regulatory effects on neutrophil extracellular traps (NETs) generation, the PAC-1/FNG/MAC-1 signaling axis, and endothelial mitochondrial function, thereby providing a theoretical basis for targeted therapeutic strategies. Methods: Peripheral blood was collected from healthy volunteers and DVT patients to assess p47phox expression, NET-related markers, and coagulation parameters. A DVT model was established using p47phox gene knockout (p47phox Results: p47phox Conclusion: Systemic p47phox deficiency suppresses DVT formation by inhibiting the PAC-1/FNG/MAC-1 signaling axis, thereby affecting platelet-neutrophil interactions and NET generation, and by protecting endothelial cells through amelioration of ROS-mediated mitochondrial dysfunction. Although
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