ArticleJournal of nanobiotechnology2026
Eosinophil-derived apoptotic extracellular vesicles accelerate steatotic liver repair after ischemia/reperfusion injury through mitochondria-associated metabolic reprogramming.
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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Abstract
Eosinophils have recently been recognized as hepatoprotective immune cells; however, cell-based therapies still face significant challenges. Apoptotic extracellular vesicles (ApoEVs) serve as critical cell-free alternatives capable of promoting tissue repair, yet exhibit marked functional heterogeneity dependent on their cell source. The therapeutic potential and mechanisms of eosinophil-derived ApoEVs (Eos-ApoEVs) in steatotic liver ischemia/reperfusion (I/R) injury remain elusive. Herein, treatment with Eos-ApoEVs effectively reversed oxygen-glucose deprivation/reperfusion (OGD/R)-induced cellular dysfunction in hepatocytes and liver sinusoidal endothelial cells (LSECs). Moreover, Eos-ApoEVs exerted potent immunomodulatory effects. Mechanistically, Eos-ApoEVs are enriched with functional mitochondria that fuse with damaged mitochondria in recipient cells, thereby reprogramming energy metabolism to promote hepatocyte proliferation, restore LSEC migration and tube-forming capacity, and facilitate anti-inflammatory macrophage polarization. To develop a clinically translatable therapeutic approach, we constructed a decellularized amniotic matrix (dAM)-based hydrogel patch (ApoEVs@dAM/HA-DA), which enables sustained release of ApoEVs and exhibits high biocompatibility. In a mouse model of steatotic liver I/R injury, transplantation of ApoEVs@dAM/HA-DA onto the liver surface significantly increased anti-inflammatory macrophage polarization, attenuated inflammation, promoted hepatocyte proliferation and enhanced angiogenesis, thereby accelerating liver repair. Thus, surface transplantation of ApoEVs@dAM/HA-DA provides a clinically viable and potent therapeutic strategy for steatotic liver I/R injury.
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