ArticleAdvanced healthcare materials2025
Immunometabolic Effect of Nitric Oxide on Human Macrophages Challenged With the SARS-CoV2-Induced Cytokine Storm. A Fluxomic Approach.
Article in Advanced healthcare materials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Nitric Oxide Synthase 2 (NOS2) Gene Polymorphisms Association With Risk of Pulmonary Tuberculosis (PTB): A Case-Control Study.BioMed research international · 2026Article
- Immunometabolic Effect of Nitric Oxide on Human Macrophages Challenged With the SARS-CoV2-Induced Cytokine Storm. A Fluxomic Approach.Advanced healthcare materials · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
The cytokine storm associated with SARS-CoV-2 infection is one of the most distinctive pathological signatures in COVID-19 patients. Macrophages respond to this pro-inflammatory challenge by reprogramming their functional and metabolic phenotypes. Interestingly, human macrophages fail to express the inducible form of the NO synthase (NOS2) in response to pro-inflammatory activation and, therefore, NO is not synthesized by these cells. The contribution of exogenously added NO, via a chemical NO-donor, on the immunometabolic changes associated with the cytokine storm is investigated. By using metabolic, transcriptomic, and functional assays the effect of NO in human macrophages is evaluated and found specific responses. Moreover, through integrative fluxomic analysis, pathways modified by NO that contribute to the expression of a particular phenotype in human macrophages are identified, which includes a decrease in mitochondrial respiration and TCA with a slight increase in the glycolytic flux. A significant ROS increase and preserved cell viability are observed in the presence of NO, which may ease the inflammatory response and host defense. Also, NO reverses the cytokine storm-induced itaconate accumulation. These changes offer additional clues to understanding the potential crosstalk between NO and the COVID-19 cytokine storm-dependent signaling pathways.
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Registered trials
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