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NO inhibits vital cellular activities including mitochondrial respiration. Mitochondrial respiration inhibition via NO occurs at discrete levels of activating stimulus, termed the mitochondrial respiration threshold, and regulation of this threshold is not fully understood. In this work, we characterize the role of uridine diphosphate glucose as a modulator of NO-mediated mitochondrial respiration inhibition via P2Y14 receptor signaling in stimulated BMDCs. We demonstrate that BMDCs exhibit an enhanced proinflammatory profile in the presence of uridine diphosphate glucose, providing evidence for a new NO regulatory axis in BMDCs. These studies highlight the importance of the growing body of literature supporting metabolites as signaling molecules in activating conditions thus allowing for better modeling of physiologically relevant contexts for myeloid cell encounters with microbial stimuli.<\/jats:p>","DOI":"10.1093\/jleuko\/qiaf047","type":"journal-article","created":{"date-parts":[[2025,4,17]],"date-time":"2025-04-17T08:32:23Z","timestamp":1744878743000},"source":"Crossref","is-referenced-by-count":1,"title":["UDP-glucose regulates dendritic cell mitochondrial respiration via a nitric oxide\u2013dependent mechanism"],"prefix":"10.1093","volume":"117","author":[{"given":"Bay","family":"Vagher","sequence":"first","affiliation":[{"name":"Cellular, Molecular, and Biomedical Sciences Graduate Program, University of Vermont , 106 Carrigan Drive, Burlington, VT 05405 ,","place":["United States"]},{"name":"Department of Biomedical and Health Sciences, University of Vermont , Rowell 302, 106 Carrigan Drive, 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