ArticleJournal of nanobiotechnology2025
Magnetically navigated nano-PROTAC ameliorates acute lung injury.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- TRIM24 stabilizes the p110 CUX1 oncoprotein via USP10 to promote chemoresistance in acute myeloid leukemia.Journal of translational medicine · 2026Article
- Review
- NIR-responsive prussian Blue/Fer-1 co-loaded nanozymes for synergistic therapy of acute lung injury.Journal of nanobiotechnology · 2026Article
- Revolutionizing protein degradation: Harnessing nanoparticles for PROTAC delivery.Materials today. Bio · 2026Review
- Activating transcription factors: Orchestrators of macrophage biology in pathological settings (Review).International journal of molecular medicine · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
introductionAcute lung injury (ALI) is an acute inflammatory lung disease with high rates of morbidity and mortality. The lack of efficient pharmacological treatments for ALI resulted in poor outcomes and prognosis.
methodsPoly(lactic-co-glycolic acid) (PLGA) was used to carry magnetic nanoparticles and TRIM24-targeted PROTAC (dTRIM24), which was further camouflaged with the exosome membranes derived from M1 macrophages to obtain nano-PROTAC (EM/PLGA/Magnetic nanoparticles/dTRIM24, EMPLANT). We evaluated the nanoparticles on the physicochemical properties, cellular uptake, in vitro toxicity, anti-inflammatory effects, in vivo biodistribution, in vivo therapeutic effect, anti-inflammatory capacity, and in vivo safety.
resultsThis nano-PROTAC EMPLANT, shows dual-targeting capability by magnetic navigation and inflammatory specificity. EMPLANT selectively accumulates in the inflammatory lungs in ALI model mice under an external magnetic field, reduces lung injuries, and drastically prolongs survival. Mechanistically, the degradation of TRIM24 upregulates the expression of STAT6 and thus promotes an efficient phenotypic switch of macrophages from M1 to M2. This strategy can ameliorate ALI greatly and increase the survival ratio to nearly 100%.
conclusionThe nano-PROTAC demonstrates a promising therapeutic strategy for ALI through precisely in situ reprogramming macrophages. To the best of our knowledge, we are the first to develop this type of magnetically navigated artificial exosomes to deliver PROTAC and use it for ALI treatment.
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