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Fatty acid\u2010binding protein 7 (FABP7), an intracellular lipid chaperone for polyunsaturated fatty acids (PUFAs), is highly expressed in liver macrophages. However, the mechanisms by which FABP7 regulates hepatic macrophage activation remain unclear. Therefore, we aimed to elucidate the mechanisms underlying the effects of FABP7 on the functions of hepatic macrophages in metabolic dysfunction\u2010associated steatohepatitis (MASH) and liver fibrosis models. In this study, we found that FABP7\u2010deficient macrophages exhibited impaired M2 polarization, which reduced the fibrotic response of myofibroblasts and CD4\n                    <jats:sup>+<\/jats:sup>\n                    T\u2010cell infiltration into the liver tissues in a carbon tetrachloride (CCl\n                    <jats:sub>4<\/jats:sub>\n                    )\u2010induced hepatic fibrosis model. In vitro, FABP7\u2010deficient macrophages exhibited decreased levels of peroxisome proliferator\u2010activated receptor (PPAR)\u2010\n                    <jats:italic>\u03b3<\/jats:italic>\n                    and its target genes, including C\u2013C motif chemokine ligand (CCL)\u201017 and transforming growth factor\u2010\n                    <jats:italic>\u03b2<\/jats:italic>\n                    (TGF\u2010\n                    <jats:italic>\u03b2<\/jats:italic>\n                    ), compared to the wild\u2010type (WT) macrophages post\u2010interleukin (IL)\u20104 stimulation. However, these effects were inhibited by a PPAR\n                    <jats:italic>\u03b3<\/jats:italic>\n                    inhibitor. IL\u20104\u2010stimulated WT macrophages also promoted CD4\n                    <jats:sup>+<\/jats:sup>\n                    T\u2010cell migration and hepatic fibroblast (TWNT\u20101 hepatic stellate cell [HSC]) activation, indicated by increased mRNA levels of actin alpha 2, smooth muscle (\n                    <jats:italic>ACTA2<\/jats:italic>\n                    ), and collagen type I alpha 1 (\n                    <jats:italic>COL1A1<\/jats:italic>\n                    ); however, these effects were inhibited in FABP7\u2010deficient macrophages. Overall, FABP7 in hepatic macrophages modulated the crosstalk between hepatic fibroblasts and T cells by regulating M2 polarization. Therefore, regulation of hepatic macrophage function by FABP7 is a potential therapeutic target for liver fibrosis.\n                  <\/jats:p>","DOI":"10.1155\/jimr\/6987981","type":"journal-article","created":{"date-parts":[[2025,2,20]],"date-time":"2025-02-20T01:31:05Z","timestamp":1740015065000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["FABP7 in Hepatic Macrophages Promotes Fibroblast Activation and CD4\n                    <sup>+<\/sup>\n                    T\u2010Cell Migration by Regulating M2 Polarization During Liver 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