ArticleBurns & trauma2025
Lipopolysaccharide-induced active telocyte exosomes alleviate lipopolysaccharide-induced vascular barrier disruption and acute lung injury via the activation of the miRNA-146a-5p/caspase-3 signaling pathway in endothelial cells.
Article in Burns & trauma, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Recent Advances in Exosome-Based Therapeutic Strategies for Acute Lung Injury: Mechanisms and Translational Advances.Antioxidants (Basel, Switzerland) · 2026Review
- Novel Hybrid Peptide DEFB126 (1-39)-TP5 Inhibits LPS-Induced Inflammatory Responses and Oxidative Stress by Neutralizing LPS and Blocking the TLR4/MD2-NFκB Signaling Axis.Antioxidants (Basel, Switzerland) · 2025Article
- Xuebijing Injection Alleviates Sepsis-Induced Acute Lung Injury by Inhibition of Cell Apoptosis and Inflammation Through the Hippo Pathway.Journal of inflammation research · 2025Article
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Authors and funding
7 authors.
Funding
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Abstract
Background: Lipopolysaccharide (LPS)-induced apoptosis of lung microvascular endothelial cells (ECs) is the main reason of lung edema and acute lung injury (ALI) in septic conditions. Telocytes (TCs) are a distinct type of interstitial cells found around the lung microvasculature, which may protect ECs through the release of shed vesicles. However, whether TCs protect against LPS-induced EC apoptosis and ALI has not been determined. Methods: The protective effects of TCs on ECs were assessed Results: We demonstrated that LPS stimulation induced the secretion of active exosomes from TCs, which inhibited LPS-mediated apoptosis of ECs and reduced ALI in mice. Moreover, miRNA-146a-5p was identified as the main bioactive molecule in TC-derived exosomes, capable of inhibiting LPS-induced caspase-3 activation and apoptosis in ECs. Conclusions: Our results indicate that TCs effectively prevent LPS-induced EC apoptosis and ALI through the release of exosomes, with subsequent activation of the miRNA-146a-5p/caspase-3 signaling pathway in ECs.
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Registered trials
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