ArticleJournal of nanobiotechnology2026
M2 macrophage-derived apoptotic vesicles alleviate liver fibrosis via miR-1224-5p-mediated inhibition of the SP1/TGF-β pathway in hepatic stellate cells.
Article in Journal of nanobiotechnology, 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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Abstract
Liver fibrosis remains a significant clinical challenge with limited therapeutic options. Apoptotic extracellular vesicles (apoVs) derived from macrophages have emerged as promising mediators of tissue repair, but their role in shaping liver fibrosis is poorly understood. Here, we demonstrate that M2 macrophage-derived apoVs (M2-apoVs) alleviate liver fibrosis by modulating hepatic stellate cells (HSCs) activation. Mechanistically, M2-apoVs deliver miR-1224-5p to HSCs, which suppresses the SP1/TGF-β pathway, thereby inhibiting fibrogenic gene expression, proliferation, and migration. In vitro, M2-apoVs reduced extracellular matrix (ECM) deposition by downregulating the expression of collagen I (Col I) and α-smooth muscle actin (α-SMA) in HSCs. Furthermore, M2-apoVs promoted the establishment of an antifibrotic microenvironment by regulating macrophage polarization and HSC-macrophage crosstalk. In a CCl₄-induced liver fibrosis mouse model, M2-apoVs treatment significantly reduced collagen accumulation and improved liver histology. Our findings revealed a novel miR-1224-5p/SP1/TGF-β regulatory axis in liver fibrosis and highlighted the therapeutic potential of M2-apoVs as a cell-free strategy for treating fibrotic liver diseases.
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