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It triggers severe disturbances in cardiovascular, neurohormonal, and metabolic homeostasis with ionic imbalance notably due to Na\n                    <jats:sup>+<\/jats:sup>\n                    \/K\n                    <jats:sup>+<\/jats:sup>\n                    \u2010ATPase dysfunction. O\u2010GlcNAcylation, a post\u2010translational modification essential for cellular protection under stress, has emerged as a promising therapeutic target in ischemia\u2010reperfusion and septic shock.\n                  <\/jats:p>\n                  <jats:p>\n                    This study aimed to determine the effects of stimulating O\u2010GlcNAcylation during HS and to clarify the related molecular mechanisms. Adult male rats were subjected to controlled HS and received either NButGT (2 injections of 10\u00a0mg\/kg) to enhance O\u2010GlcNAcylation or saline. Hemodynamic parameters and plasmatic markers of organ injury were assessed after 24 h. O\u2010GlcNAcylation levels, protein expression, and Na\n                    <jats:sup>+<\/jats:sup>\n                    \/K\n                    <jats:sup>+<\/jats:sup>\n                    \u2010ATPase O\u2010GlcNAcylation were analyzed via Western blot and immunofluorescence, while Na\n                    <jats:sup>+<\/jats:sup>\n                    \/K\n                    <jats:sup>+<\/jats:sup>\n                    \u2010ATPase activity was measured by colorimetry. NButGT increased cardiac and renal O\u2010GlcNAcylation levels, improved hemodynamic and reduced organ damage. HS disrupts electrolyte homeostasis with decreased bicarbonate and sodium levels and elevated potassium concentration. NButGT administration restored ionic balance and renal Na\n                    <jats:sup>+<\/jats:sup>\n                    \/K\n                    <jats:sup>+<\/jats:sup>\n                    \u2010ATPase expression. Treatment with NButGT elevated Na\n                    <jats:sup>+<\/jats:sup>\n                    \/K\n                    <jats:sup>+<\/jats:sup>\n                    \u2010ATPase activity. These results demonstrate that acute O\u2010GlcNAcylation stimulation supports physiological recovery in HS by promoting ionic homeostasis and Na\n                    <jats:sup>+<\/jats:sup>\n                    \/K\n                    <jats:sup>+<\/jats:sup>\n                    \u2010ATPase function.\n                  <\/jats:p>","DOI":"10.1002\/mco2.71056","type":"journal-article","created":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T05:19:39Z","timestamp":1791782379000},"source":"Crossref","is-referenced-by-count":0,"title":["O\u2010GlcNAcylation Stimulation Modulates Na+\/K+ ATPase and Improves Outcomes in Hemorrhagic Shock"],"prefix":"10.1002","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8827-3526","authenticated-orcid":false,"given":"Thomas","family":"Dupas","sequence":"first","affiliation":[{"name":"Nantes Universit\u00e9, CHU Nantes, CNRS, INSERM, L'institut Du Thorax  Nantes 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