ArticleJournal of nanobiotechnology2025
Promotion of NLRP3 autophagosome degradation by PV-K nanodevice for protection against macrophage pyroptosis-mediated 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. An erratum has been issued. 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.
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Who cites it
4 citing papers in PubMed.
- Mechanisms and therapeutic strategies of pyroptosis in sepsis‑induced acute lung injury (Review).International journal of molecular medicine · 2026Review
- GPR43 alleviates LPS-induced acute lung injury by inhibiting NLRP3 inflammasome activation via β-arrestin 2.Biology direct · 2026Article
- NLRP3 inflammasomes at the ARDS-cancer interface: mechanisms and translational hypotheses.Frontiers in immunology · 2026Review
- Regulated programmed cell death in acute lung injury: from pathogenesis to therapy.Frontiers in immunology · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
17 authors.
Funding
Abstract
Acute respiratory distress syndrome (ARDS) has emerged as a significant global health challenge, with no definitive curative treatment available. Recent evidence suggests that pyroptosis of immune cells plays a pivotal role in the pathogenesis of ARDS. Targeting and modulating immune cell pyroptosis in lung tissue may offer a promising strategy to mitigate the harmful inflammation associated with this condition. In this study, we designed and synthesized a novel class of peptide-functionalized nanoparticles, PV-K, which possess an intrinsic capacity for phagocytosis by macrophages. Concurrently, the incorporation of two FFD functional groups into a single polypeptide enhances the biological activity of PV-K. Amazingly, PV-K demonstrated potent inhibitory effects on nucleotide-binding domain, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3)-mediated pyroptosis in both mouse bone marrow-derived macrophages and the human THP-1 cell-derived macrophages. In both lipopolysaccharide and cecal ligation and puncture induced acute lung injury mouse models, treatment with PV-K significantly reduced disease severity by alleviating pulmonary inflammation and inhibiting macrophage pyroptosis. Transcriptomic analysis revealed that PV-K enhanced SQSM1/p62-mediated autophagy through upregulation of the NRF2 signaling pathway. Mechanistically, PV-K facilitated the interaction between SQSTM1/p62 and NLRP3, promoting the autolysosomal degradation of NLRP3. Notably, the inhibitory effect of PV-K on macrophage pyroptosis during acute lung injury was abrogated in Nrf2
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