ArticleJournal of nanobiotechnology2024
Macrophage biomimetic nanoparticle-targeted functional extracellular vesicle micro-RNAs revealed via multiomics analysis alleviate sepsis-induced acute lung injury.
Article in Journal of nanobiotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Review
- Targeting the NR1D1-IGF2BP2-V-ATPase Axis With Hybrid Nanovesicles Restores Macrophage Rhythms to Reverse Sepsis-Induced Immunosuppression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Bioactive co-assembly of PSA/diT-VES nanomicelles orchestrates macrophage reprogramming for acute lung injury therapy.Drug delivery and translational research · 2026Article
- The role of immunomodulatory nano systems in the treatment of sepsis: past, present, and future.Nanomedicine (London, England) · 2026Review
- Gasdermin D-driven pyroptosis in sepsis: mechanisms, therapeutic strategies, and clinical translation.Frontiers in immunology · 2026Review
- Interaction networks of macrophage glycolysis and inflammation in sepsis: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Decoding the lncRNA-miRNA-mRNA network in sepsis-induced lung injury: from pathogenesis to extracellular vesicle-based therapy.Frontiers in immunology · 2026Review
- Macrophage Hypoxia Signaling Pathways and Their Roles in Sepsis.Journal of inflammation research · 2026Review
- miRNAs-neutrophil axis: novel insights into acute lung injury and chronic inflammatory lung diseases.Frontiers in immunology · 2026Review
- Extracellular vesicles as emerging platforms for modulating innate immune responses in sepsis-associated acute lung injury.Frontiers in immunology · 2026Review
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Spermidine Alleviates Sepsis-Induced Acute Lung Injury through AMPK-Mediated Improvement of Necroptosis.Inflammation · 2025Article
- Engineered immune-driven theranostics for clinical cardiology.Military Medical Research · 2025Review
- Extracellular Vesicles in Calcific Aortic Valve Disease: From Biomarkers to Drug Delivery Applications.Biomolecules · 2025Review
- Inflammatory cytokine-primed MSC-derived extracellular vesicles ameliorate acute lung injury via enhanced immunomodulation and alveolar repair.Stem cell research & therapy · 2025Article
- Selenium nanoparticles activate selenoproteins to mitigate septic lung injury through miR-20b-mediated RORγt/STAT3/Th17 axis inhibition and enhanced mitochondrial transfer in BMSCs.Journal of nanobiotechnology · 2025Article
- Advancements in omics technologies: Molecular mechanisms of acute lung injury and acute respiratory distress syndrome (Review).International journal of molecular medicine · 2025Review
- Immune-modulatory biomimetic nanoparticles: Advances in design, mechanisms, and nanomedicine applications.BioImpacts : BI · 2025Article
- Editorial: The immunological events of macrophages in the course of sepsis.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Patients who suffer from sepsis typically experience acute lung injury (ALI). Extracellular vesicles (EVs) contain miRNAs, which are potentially involved in ALI. However, strategies to screen more effective EV-miRNAs as therapeutic targets are yet to be elucidated. In this study, functional EV-miRNAs were identified based on multiomics analysis of single-cell RNA sequencing of targeted organs and serum EV (sEV) miRNA profiles in patients with sepsis. The proportions of neutrophils and macrophages were increased significantly in the lungs of mice receiving sEVs from patients with sepsis compared with healthy controls. Macrophages released more EVs than neutrophils. MiR-125a-5p delivery by sEVs to lung macrophages inhibited Tnfaip3, while miR-221-3p delivery to lung neutrophils inhibited Fos. Macrophage membrane nanoparticles (MM NPs) loaded with an miR-125a-5p inhibitor or miR-221-3p mimic attenuated the response to lipopolysaccharide (LPS)-induced ALI. Transcriptome profiling revealed that EVs derived from LPS-stimulated bone marrow-derived macrophages (BMDMs) induced oxidative stress in neutrophils. Blocking toll-like receptor, CXCR2, or TNFα signaling in neutrophils attenuated the oxidative stress induced by LPS-stimulated BMDM-EVs. This study presents a novel method to screen functional EV-miRNAs and highlights the pivotal role of macrophage-derived EVs in ALI. MM NPs, as delivery systems of key sEV-miRNA mimics or inhibitors, alleviated cellular responses observed in sepsis-induced ALI. This strategy can be used to reduce septic organ damage, particularly lung damage, by targeting EVs.
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