ArticleiScience2025
Inflammation-responsive biomimetic nanoparticles with epigallocatechin-3-gallate for acute lung injury therapy via autophagy enhancement.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Cycloastragenol reduces inflammation and apoptosis in acute lung injury by inhibiting the NF-κB p65 and Akt pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Applications of Tailored Mesoporous Silicate Nanomaterials in Regenerative Medicine and Theranostics.International journal of molecular sciences · 2025Review
- Luteolin attenuates inflammation and apoptosis in LPS-induced ALI mice by activating the HGF/c-Met pathway.Frontiers in pharmacology · 2025Article
- Targeting immune cell migration as therapy for inflammatory disease: a review.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) is a severe inflammatory condition that can rapidly progress to acute respiratory distress syndrome, causing irreversible tissue damage. Effective anti-inflammatory and antioxidant therapies are crucial for treating ALI. We developed a dual inflammatory targeting and immune evasion capability nanoparticle, which combines epigallocatechin-3-gallate (EGCG) loaded into mercaptoketone (TK)-functionalized mesoporous silica (MSN) and coated with platelet-neutrophil hybrid membranes (PNMs). PNM-EGCG@MSN-TK nanoparticles enhance targeting to inflammatory sites and specifically remove high levels of reactive oxygen species (ROS) in cells. They also release EGCG in response to high ROS levels, improving cellular oxidative stress and enhancing autophagy in lung epithelial cells via the MAPK/BNIP3 pathway. This approach effectively ameliorates acute lung injury, suggesting a promising therapeutic strategy for ALI treatment.
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Registered trials
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