ArticleBMJ open respiratory research2023
Fibrotic extracellular vesicles contribute to mechanical ventilation-induced pulmonary fibrosis development by activating lung fibroblasts via JNK signalling pathway: an experimental study.
Article in BMJ open respiratory research, 2023. 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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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
3 citing papers in PubMed, 5 citations in OpenAlex.
- Effects of mechanical ventilation on the interstitial extracellular matrix in healthy lungs and lungs affected by acute respiratory distress syndrome: a narrative review.Critical care (London, England) · 2024Review
- Mendelian randomisation highlights type 1 diabetes as a causal determinant of idiopathic pulmonary fibrosis.Diabetology & metabolic syndrome · 2024Article
- Role of Exosomes in Epithelial-Mesenchymal Transition.ACS applied bio materials · 2024Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent research has revealed that mechanical ventilation (MV) could initiate ventilator-induced lung injury along with the initiation of the process of pulmonary fibrosis (PF), leading to MV-induced PF (MVPF). However, the underlying mechanism remains unclear. This study aimed to explore the role of MV-induced extracellular vesicles (MV-EVs) and the c-Jun N-terminal kinase (JNK) signalling pathway in the pathogenesis of MVPF in vivo and in vitro. The process of MV is accompanied by the secretion of MV-EVs, which could induce lung fibroblast activation. Furthermore, single-cell RNA-sequencing analysis revealed that the JNK pathway in lung fibroblasts was activated after MV initiation. Inhibiting the JNK pathway could both restrain MV-EV-induced lung fibroblast activation in vitro or reduce the severity of MVPF in vivo. In conclusion, this study demonstrated that MV-EVs contribute to MVPF progression by activating lung fibroblasts via the JNK signalling pathway and that inhibiting the secretion of EV and the activation of the JNK signalling pathway is a promising strategy for treating MVPF.
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