ArticleStem cell research & therapy2025
MiR-24-3p delivered by adipose derived stem cells exosomes alleviate macrophage pyroptosis via NLRP3/Caspase1/GSDMD in sepsis ALI.
Article in Stem cell research & therapy, 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.
- Programmed cell death in metabolic syndrome: From molecular mechanisms to therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- Targeting perivascular adipose tissue in vascular aging: innovative translational strategies for disease prevention and monitoring.Apoptosis : an international journal on programmed cell death · 2026Review
- Recent Advances in Exosome-Based Therapeutic Strategies for Acute Lung Injury: Mechanisms and Translational Advances.Antioxidants (Basel, Switzerland) · 2026Review
- From nanotechnology to immunomodulation: emerging strategies targeting macrophages in high altitude pulmonary hypertension.Journal of nanobiotechnology · 2026Review
- Single-cell RNA-Seq reveals transcriptional heterogeneity in sepsis and down-regulation of SNHG5/miR-324-5p/CDK16 axis in T cells.Cell biology and toxicology · 2026Article
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Authors and funding
14 authors.
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Abstract
backgroundSepsis is a life-threatening condition associated with high morbidity and mortality, frequently resulting in acute lung injury (ALI) as one of its most severe complications. The pathogenesis of sepsis-induced ALI is significantly influenced by excessive inflammation, particularly that mediated by macrophages, plays a critical role in the pathogenesis of sepsis-induced ALI. This study sought to explore the protective effects and underlying mechanisms of adipose-derived stem cell exosomes (ADSCs-exo) on macrophage-mediated inflammation and pyroptosis.
methodsADSCs-exo were isolated and characterized using nanoparticle tracking analysis (NTA), Western blotting, and transmission electron microscopy. A macrophage pyroptosis model was established through lipopolysaccharide (LPS) stimulation. The effects of ADSCs-exo on the secretion of inflammatory cytokine and pyroptosis-related markers (NLRP3, Caspase1, GSDMD) was evaluated. Mechanistic studies included dual-luciferase reporter assays and NLRP3 inhibition experiments. In vivo, a cecal ligation and puncture (CLP) sepsis model was utilized to evaluate the impact of ADSCs-exo on pulmonary inflammation, histopathological damage, survival rates, macrophage polarization (M1/M2), and components of the pyroptosis pathway (NLRP3, Caspase1).
resultsIsolated ADSCs-exo displayed characteristic features of exosomes. The administration of ADSCs-exo mitigated LPS-induced hyperinflammation in macrophages, which was associated with a decreased expression of pyroptosis executors, namely Caspase1, GSDMD and NLRP3. Mechanistically, ADSCs-exo facilitated the delivery of miR-24-3p, which specifically targeted NLRP3 to inhibit pyroptosis. In mice subjected to CLP-challenge, the administration of ADSCs-exo improved lung pathology, enhanced survival rates, and reduced markers of pyroptosis in pulmonary tissues.
conclusionsOur findings indicate that ADSCs-exo attenuates ALI by modulating macrophage pyroptosis through the miR-24-3p/NLRP3/Caspase1/GSDMD axis, thereby presenting a promising therapeutic approach for sepsis-associated ALI.
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