ReviewiLIVER2026
Heterogeneity of hepatic macrophages in MASLD/MASH: Lipid-associated programs, molecular mechanisms, spatial niches, and therapeutic implications.
Review in iLIVER, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
7 authors.
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Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), are leading causes of chronic liver disease worldwide. Increasing evidence indicates that hepatic macrophages play central roles in disease development and resolution. However, their functional heterogeneity has only recently been recognized. Hepatic macrophages consist of embryonically derived Kupffer cells and monocyte-derived macrophages, which undergo dynamic phenotypic and metabolic remodeling in response to lipid overload, inflammation, and tissue injury. Recent single-cell, spatial, and multi-omics studies have identified lipid-associated macrophages (LAMs) as a distinct macrophage program enriched in MASLD/MASH. LAMs are characterized by enhanced lipid-handling capacity, lysosomal activation, and lipid-sensing transcriptional programs involving triggering receptor expressed on myeloid cells 2 (TREM2), peroxisome proliferator-activated receptor γ, liver X receptor α, and microphthalmia-associated transcription factor. Spatially, TREM2
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