ArticleFrontiers in immunology2025
Phospholipase D1 is a critical mediator of neutrophil extracellular trap formation and venous thrombosis.
Article in Frontiers in immunology, 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.
- Machine Learning-Based Prediction of Lower Extremity Deep Vein Thrombosis in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease.International journal of general medicine · 2026Article
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Authors and funding
10 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Neutrophil extracellular traps (NETs) are a host defense mechanism whereby activated neutrophils release decondensed chromatin and antimicrobial proteins into the extracellular space to trap and kill invading pathogens. While effective in clearing pathogens, NETs also pose pathological risks by exposing self-DNA, histones, granular enzymes, and reactive oxygen species (ROS), contributing to pathologies such as autoimmune diseases, inflammatory disorders, and thrombosis. Here, we identify phospholipase D1 (PLD1), a lipid-signaling enzyme that generates phosphatidic acid (PA), as a critical regulator of ROS generation and NET formation in murine neutrophils. Using both PLD1-deficient neutrophils and a selective inhibitor, we demonstrate that PLD1 is essential for NET release. Notably, exogenous PA alone is sufficient to trigger robust ROS production and NET formation.
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