ArticleProceedings of the National Academy of Sciences of the United States of America2024
Hyponatremia unleashes neutrophil extracellular traps elevating life-threatening pulmonary embolism risk.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Neutrophil-based immunotherapy: A metabolic lens on mechanisms and therapeutic implications.Clinical and translational medicine · 2026Review
- Severity-Stratified Hyponatremia Is Associated with Increased Mortality and Complications in Nontraumatic Intracerebral Hemorrhage.Journal of clinical medicine · 2026Article
- Regulation of bone immunity by metal ions: a review of mechanisms and application progress.Frontiers in immunology · 2026Review
- Independent and combined predictive value of nutritional, electrolyte, inflammatory, and insulin resistance indices for post-stroke infection in acute ischemic stroke: a retrospective study.Frontiers in nutrition · 2026Article
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Authors and funding
7 authors.
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Abstract
Neutrophil extracellular traps (NETs), essential for controlling infections, can induce various pathologies when dysregulated. Known triggers for infection-independent NETs release exist, yet a comprehensive understanding of the conditions prompting such responses is lacking. In this study, we identify hyponatremia as an independent inducer of NETs release, a common clinical condition that disrupts sodium/calcium exchange within neutrophils. This disruption leads to an excess of intracellular calcium, subsequent elevation of reactive oxygen species (ROS), and the citrullination of histone H3, culminating in the activation of NETs-release pathways. Notably, under hyponatremic conditions, this mechanism is exacerbated during infectious states, leading to the deposition of NETs in the lungs and increasing the risk of life-threatening pulmonary embolism. Our findings underscore the critical role of sodium and calcium homeostasis in neutrophil functionality and provide insights into the pathogenesis of hyponatremia-associated diseases, highlighting potential therapeutic interventions targeting NETs dynamics.
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