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The zonal loss of Kit in liver sinusoidal endothelial cells (LSECs) during MASH suggests a role in niche maintenance, but its regulatory function is unclear. This study aimed to define how the zonated LSEC Kit controls macrophage distribution in MASH.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods<\/jats:bold>\n                    : We used zonal LSEC isolation, endothelial\u2010specific knockout mice, spatial transcriptomics, and human data to dissect this axis.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results<\/jats:bold>\n                    : Pericentral LSEC Kit maintains homeostasis by suppressing FSTL1 via STAT2 phosphorylation. In MASH, Kit loss triggers centrilobular FSTL1 upregulation. The resulting FSTL1 gradient drives centrilobular accumulation of pro\u2010inflammatory ITGA4\n                    <jats:sup>+<\/jats:sup>\n                    macrophages via NF\u2010\u03baB. Inhibiting FSTL1 or ITGA4 restored macrophage zonation and ameliorated MASH.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion<\/jats:bold>\n                    : The Kit\/STAT2\/FSTL1\/ITGA4 axis is a master regulator of inflammatory zonation in MASH, revealing how zonal endothelial dysfunction drives spatial immune reorganization and offering a new framework for therapy.\n                  <\/jats:p>","DOI":"10.1002\/advs.76410","type":"journal-article","created":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T13:46:46Z","timestamp":1785764806000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Liver Endothelia Orchestrate MASH\u2010Associated Macrophage Zonation Through FSTL1\u2010ITGA4 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