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Here, we investigated myeloid HDAC7 functions in obesity\u2010driven metabolic disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We used gain\u2010 and loss\u2010of\u2010function genetic approaches in mice to investigate myeloid HDAC7 functions in hepatic inflammation and metabolic disease, as well as associations with hepatic gene signatures characteristic of advanced chronic liver disease (CLD).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Transgenic expression of\n                      <jats:italic>Hdac7<\/jats:italic>\n                      in myeloid cells increased liver inflammation and liver mRNA levels of\n                      <jats:italic>Ccl2<\/jats:italic>\n                      and\n                      <jats:italic>Il1b<\/jats:italic>\n                      , key inflammatory mediators linked to CLD. Liver glycogen levels were also decreased, another feature of CLD. Transgenic expression of\n                      <jats:italic>Hdac7<\/jats:italic>\n                      in myeloid cells mimicked the hepatic inflammatory phenotype that was observed in mice fed a high fat, high cholesterol and high sucrose (HFHCHS) diet, an obesity model that mimics some features of metabolic dysfunction\u2010associated steatotic liver disease. In myeloid\n                      <jats:italic>Hdac7<\/jats:italic>\n                      transgenic mice fed a HFHCHS diet, relative weight gain was increased, fasted glucose levels were elevated, and glucose tolerance was dysregulated by comparison to control mice. Conversely, fasted blood glucose levels were reduced and glucose tolerance was improved in myeloid\n                      <jats:italic>Hdac7<\/jats:italic>\n                      \u2010deleted mice on a HFHCHS diet.\n                      <jats:italic>HDAC7<\/jats:italic>\n                      mRNA levels were also elevated in the livers of people with advanced CLD and spatial transcriptomics revealed that myeloid HDAC7 directs hepatic gene signatures characteristic of advanced CLD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Myeloid HDAC7 contributes to hepatic inflammation and systemic glucose dysregulation in a mouse model of obesity and liver inflammation.<\/jats:p>\n                  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