ArticleDiscover oncology2026
Hepatic stellate cell derived lipid droplets drive protumoral M2 macrophage polarization in hepatocellular carcinoma.
Article in Discover oncology, 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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Abstract
backgroundDuring chronic liver injury, hepatic stellate cells (HSCs) lose their vitamin-A-rich lipid droplets (LDs), yet whether these organelles are merely degraded or released via vesicles and functionally relevant remains unclear. We investigated the fate of HSCs LDs and their impact on hepatic macrophage phenotype and hepatocellular carcinoma (HCC) development.
methodsChronic liver injury was induced in C57BL/6 mice using carbon tetrachloride (CCl
resultsActivated HSCs in fibrotic livers showed progressive fragmentation and release of LDs, which were subsequently internalized by hepatic macrophages. Single-cell transcriptomic analysis revealed enhanced HSC-macrophage interactions and upregulation of lipid metabolism pathways in both cell types during liver inflammation. HSC-derived LDs acted as a direct metabolic cue to induced M2 polarization of macrophages, characterized by elevated secretion of transforming growth factor-beta (TGF-β1), interleukin-10 (IL-10), and C-C Motif Chemokine Ligand 17 (CCL17). In orthotopic HCC models, co-injection of tumor cells with lipid droplet-educated macrophages significantly enhanced tumor growth compared to control macrophages. TCGA analysis showed that high CD163 expression correlated with poor overall survival in HCC patients.
conclusionOur findings identifies a distinct mechanism whereby activated HSCs transfer LDs to hepatic macrophages, inducing M2 polarization and creating a pro-tumorigenic microenvironment. This HSC-macrophage crosstalk represents a potential metabolic therapeutic target for preventing HCC development in patients with chronic liver disease.
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