ArticleFrontiers in physiology2025
Nitroalkene inhibition of pro-inflammatory macrophage effector function via modulation of signaling metabolite levels.
Article in Frontiers in physiology, 2025. 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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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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10 authors.
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Abstract
Introduction: Classically activated innate immune cells undergo a metabolic switch to aerobic glycolysis to support effector function. We report that the small-molecule nitroalkene 10-n-octadec-9-enoic acid (NO Methods: RAW264.7 and bone marrow derived macrophage were treated with LPS with and without NO Results: Overall, the present observations indicate that nitroalkene-induced changes in central carbon metabolism contribute to the anti-inflammatory actions of this class of multi-target lipid signaling mediators. Comparison of macrophage responses to NO Conclusion: The current data provide additional perspective on the actions of this small-molecule electrophile, which is currently in a Phase 2 clinical trial for the treatment of obesity-related chronic pulmonary inflammation and associated airway dysfunction.
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