{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T04:58:52Z","timestamp":1781240332627,"version":"3.54.1"},"reference-count":59,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T00:00:00Z","timestamp":1781222400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100012659","name":"Foundation for Innovative Research Groups of the National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82371929,  82472046"],"award-info":[{"award-number":["82371929,  82472046"]}],"id":[{"id":"10.13039\/501100012659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Hypoxic-ischemic brain damage (HIBD) involves profound metabolic reprogramming, where aberrant glycolysis links to neuronal injury. This study aimed to identify and characterize glycolysis-related hub genes in HIBD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Glycolysis-related differentially expressed genes (DEGs) were screened from the HIBD dataset GSE144456 by combining differential expression analysis, weighted gene co-expression network analysis (WGCNA), and a glycolysis gene set. Hub genes were further identified via enrichment and protein-protein interaction (PPI) network analyses and validated in an independent dataset (GSE23317) and our internal RNA-seq. The key hub gene was confirmed in a mouse HIBD model using RT-qPCR and Western blot. To perturb Hexokinase 2 (\n                      <jats:italic>Hk2<\/jats:italic>\n                      ), 3-bromopyruvate (3-BrPA, 1 mg\/kg) was administered 1 hour post-HIBD, and its effects were evaluated by MRI, molecular assays, and behavioral tests.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Bioinformatics analysis identified\n                      <jats:italic>Hk2<\/jats:italic>\n                      as a key hub gene that was consistently upregulated in HIBD.\n                      <jats:italic>In vivo<\/jats:italic>\n                      experiments demonstrated that both HK2 protein and mRNA levels were significantly elevated 24 hours after HIBD (P &amp;lt; 0.001). Double immunofluorescence staining further revealed that the upregulated HK2 was predominantly localized to Iba1\n                      <jats:sup>+<\/jats:sup>\n                      microglia. Early administration of 3-BrPA reduced acute cerebral infarction volume (P &amp;lt; 0.001), improved neurological function scores (P &amp;lt; 0.001), and concurrently\u200b downregulated HK2 protein levels (P &amp;lt; 0.05). 3-BrPA treatment also significantly reduced lactate accumulation in the injured brain tissue (P &amp;lt; 0.001). \u200bIt also\u200b suppressed the mRNA expression of pro-inflammatory cytokines (\n                      <jats:italic>Tnf<\/jats:italic>\n                      ,\n                      <jats:italic>Il1b<\/jats:italic>\n                      , and\n                      <jats:italic>Il6<\/jats:italic>\n                      ; all P &amp;lt; 0.001) and modulated the protein levels of inflammatory markers (iNOS, ARG1; P &amp;lt; 0.05 and P &amp;lt; 0.01, respectively). Moreover, this single early intervention significantly mitigated long-term brain tissue loss and improved motor coordination and exploratory behavior at 30 days post-injury (P &amp;lt; 0.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Hk2<\/jats:italic>\n                      is highlighted as a critical node associated with both glycolytic reprogramming and neuroinflammation in HIBD, with upregulation primarily in microglia. Early perturbation of glycolysis with 3-BrPA is associated with multifaceted benefits. Our findings link the\n                      <jats:italic>Hk2<\/jats:italic>\n                      -glycolysis axis to neuroinflammation, offering a rationale for exploring metabolic interventions in HIBD.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1837728","type":"journal-article","created":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T04:41:26Z","timestamp":1781239286000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Hexokinase 2 upregulation is associated with glycolytic reprogramming and neuroinflammation in hypoxic-ischemic brain damage: a therapeutic target for early intervention"],"prefix":"10.3389","volume":"17","author":[{"given":"Yue","family":"Li","sequence":"first","affiliation":[{"name":"Department of Radiology, The Third Affiliated Hospital of Zhengzhou University","place":["Zhengzhou, China"]},{"name":"Department of Clinical Research and 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