{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T20:14:50Z","timestamp":1791404090152,"version":"4.3.3"},"reference-count":36,"publisher":"MDPI AG","issue":"5","license":[{"start":{"date-parts":[[2023,4,29]],"date-time":"2023-04-29T00:00:00Z","timestamp":1682726400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"University of Alaska Fairbanks"},{"name":"establishment grant of Dr Alireza Badiei"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Biomolecules"],"abstract":"<jats:p>This study investigated the critical role of Glut1-mediated glucose metabolism in the inflammatory response of macrophages, which are energy-intensive cells within the innate immune system. Inflammation leads to increased Glut1 expression, ensuring sufficient glucose uptake to support macrophage functions. We demonstrated that using siRNA to knock down Glut1 reduces the expression of various pro-inflammatory cytokines and markers, such as IL-6, iNOS, MHC II\/CD40, reactive oxygen species, and the hydrogen sulfide (H2S)-producing enzyme cystathionine \u03b3-lyase (CSE). Glut1 activates a pro-inflammatory profile through a nuclear factor (NF)-\u03baB, while silencing Glut1 can prevent lipopolysaccharide (LPS)-induced I\u03baB degradation, blocking NF-\u03baB activation. Glut1\u2019s role in autophagy, an essential process for macrophage functions such as antigen presentation, phagocytosis, and cytokine secretion, was also measured. The findings show that LPS stimulation decreases autophagosome formation, but Glut1 knockdown reverses this effect, increasing autophagy beyond control levels. The study highlights Glut1\u2019s importance in macrophage immune responses and its regulation of apoptosis during LPS stimulation. Knocking down Glut1 negatively impacts cell viability and mitochondrial intrinsic pathway signaling. These findings collectively suggest that targeting macrophage glucose metabolism through Glut1 could potentially serve as a target for controlling inflammation.<\/jats:p>","DOI":"10.3390\/biom13050770","type":"journal-article","created":{"date-parts":[[2023,5,1]],"date-time":"2023-05-01T13:54:46Z","timestamp":1682949286000},"page":"770","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["Glucose Transporter Glut1-Dependent Metabolic Reprogramming Regulates Lipopolysaccharide-Induced Inflammation in RAW264.7 Macrophages"],"prefix":"10.3390","volume":"13","author":[{"given":"Alex","family":"Cornwell","sequence":"first","affiliation":[{"name":"Department of Biology and Wildlife, College of Natural Science and Mathematics, University of Alaska Fairbanks, Fairbanks, AK 99775, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9314-8666","authenticated-orcid":false,"given":"Hubert","family":"Zi\u00f3\u0142kowski","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Warmia and Mazury in Olsztyn, Oczapowskiego 13, 10-718 Olsztyn, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5692-091X","authenticated-orcid":false,"given":"Alireza","family":"Badiei","sequence":"additional","affiliation":[{"name":"Department of Veterinary Medicine, College of Natural Science and Mathematics, University of Alaska Fairbanks, Fairbanks, AK 99775, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,4,29]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"614","DOI":"10.3389\/fimmu.2014.00614","article-title":"Molecular Mechanisms That Influence the Macrophage M1-M2 Polarization Balance","volume":"5","author":"Wang","year":"2014","journal-title":"Front. 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