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Here, we established an ACLF mouse model recapitulating clinical hallmarks and performed single\u2010cell RNA sequencing (scRNA\u2010seq) on hepatic non\u2010parenchymal cells (NPCs). We identified 30 cell clusters and observed profound spatial remodeling of NPCs driven by pro\u2010inflammatory mediators. Endothelial cells (ECs) underwent a critical transition from homeostasis to dysfunction, marked by mitochondrial damage and activation of NF\u2010\u03baB and MAPK pathways. Ligand\u2013receptor interactome analysis identified dysfunctional ECs as central hubs driving global network reconfiguration, primarily via the\n                    <jats:italic>Lgals9\u2013Ighm\/Cd45\/Cd44<\/jats:italic>\n                    axes, alongside the suppression of homeostatic signals (\n                    <jats:italic>Cd55<\/jats:italic>\n                    and\n                    <jats:italic>APP<\/jats:italic>\n                    ). Furthermore, we mapped B cell lineage trajectories and validated the spatial co\u2010localization of EC and B\u2010cell interactions through Lgals9\u2013Ighm. This study defines the EC and B\u2010cell communication landscape and suggests that the Lgals9\u2013Ighm axis may play a critical role in ACLF progression, representing a potential candidate for therapeutic intervention.\n                  <\/jats:p>","DOI":"10.1155\/jimr\/5421823","type":"journal-article","created":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T13:18:50Z","timestamp":1788182330000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Single\u2010Cell Analysis of Hepatic Non\u2010Parenchymal Cells Reveals Endothelial Dysfunction and Altered Endothelial and B Cell Communication in Acute\u2010on\u2010Chronic Liver 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