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To address this, we integrated single\u2010cell and spatial transcriptomics with chromatin accessibility profiling, proteomics, and bulk RNA\u2010seq, then validated key findings in clinical LT specimens, mouse HIRI models, and in vitro assays. Across datasets, HIRI disproportionately aggravated pericentral hepatocyte injury and markedly coincided with heightened macrophage crosstalk. Mechanistically, we identified FOXO1\u2010dominated SAA secretion from pericentral hepatocytes that promotes FPR2\n                    <jats:sup>+<\/jats:sup>\n                    macrophages recruitment and activation, thereby exacerbating pericentral\u2010predominant hepatocyte injury. Supporting this mechanism, pharmacological inhibition of SAA\u2010driven proinflammatory activity using the SAA inhibitor Amilo\u20105MER reduced macrophage accumulation, alleviated pericentral hepatocyte damage, and mitigated zonal disparities. 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