ArticleJournal of nanobiotechnology2026
GGT-triggered self-immolative dexamethasone-oligopeptide prodrug nanoparticles ameliorate hepatic fibrosis via dual anti-inflammatory/immunomodulatory pathways with minimized systemic toxicity.
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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13 authors.
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Abstract
Liver fibrosis remains a critical unmet medical challenge, where glucocorticoids' therapeutic potential is constrained by systemic toxicity. We innovatively address this through an amphiphilic prodrug (DEI) engineered by Michael addition-conjugating dexamethasone with I-C-F-6, which self-assembles into γ-glutamyltranspeptidase (GGT)-responsive nanoparticles for liver-targeted delivery. This nanoplatform achieves spatial precision through enzyme-triggered drug self-immolative release exclusively in fibrotic livers, minimizes systemic toxicity, and modulates fibrosis pathogenesis via dual pathways. DEI-NPs could suppress hepatic stellate cell activation via TGF-β/Smad3 and TH17 pathway blockade to halt collagen I/IV deposition, and reprogram intrahepatic immunity through retinol metabolism-mediated TH17/Treg rebalancing (Cyp2a1↓/STAT1↑). Our work pioneers a paradigm-shifting strategy in glucocorticoid therapy that merges GGT-activated spatial control with immunometabolic reprogramming, effectively overcoming critical bottlenecks in fibrosis therapy.
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