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Background <p>Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a critical respiratory disorder. Clinically, ALI/ARDS patients with concurrent obesity exhibit a lower mortality rate. Epithelial-mesenchymal transition (EMT) contributes to pulmonary fibrosis and poor prognosis in patients with ALI/ARDS. This study was designed to explore the specific effects and underlying mechanism of adipose-derived exosomes (ADEs) on pulmonary EMT using an ALI model.</p> Methods <p>After administering ADEs isolated from DIO and Lean mice to the LPS-induced ALI/ARDS model, pulmonary fibrosis degree was assessed. Then, transcriptomic analysis was performed to identify candidate molecules associated with pulmonary fibrosis, and their expression levels were detected in lung tissue samples and MLE-12 cells.</p> Results <p>LPS exposure induced severe pathological damages to lung tissue, and ADEs intervention significantly alleviated pulmonary injury induced by LPS. Transcriptomic analysis demonstrated that ADEs treatment substantially affected multiple processes of the Wnt/β-catenin/Snail pathway associated with EMT. In ALI/ARDS mouse lungs and TGF-β1-treated MLE-12 cells, ADEs administration downregulated the expression levels of Wnt3a, β-catenin, Snail and Vimentin, while upregulating the expressions of E-cadherin and p-β-catenin. Furthermore, throughout the entire experimental procedure, the anti-EMT effect of DIO-Exo outperformed that of Lean-Exo in both in vivo and in vitro settings.</p> Conclusions <p>ADEs isolated from DIO mice may potentially suppress EMT in alveolar type II epithelial cells and lung tissue in the ALI/ARDS model, possibly in association with reduced Wnt/β-catenin/Snail signalling cascade. These findings offer a promising therapeutic direction for alleviating pulmonary fibrosis associated with ALI/ARDS.</p>

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Adipose-derived exosomes alleviate ALI via inhibiting epithelial-mesenchymal transition of alveolar type II cells by Wnt/β-catenin/snail pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月1日

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  • Yijian Yan,
  • Kejie Chen,
  • Mantong Zhang,
  • Ruinan Peng,
  • Danning Zhao,
  • Shan Zhang,
  • Miaomiao Zou,
  • Haibo Feng,
  • Fengyuan Wang

摘要

Background

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a critical respiratory disorder. Clinically, ALI/ARDS patients with concurrent obesity exhibit a lower mortality rate. Epithelial-mesenchymal transition (EMT) contributes to pulmonary fibrosis and poor prognosis in patients with ALI/ARDS. This study was designed to explore the specific effects and underlying mechanism of adipose-derived exosomes (ADEs) on pulmonary EMT using an ALI model.

Methods

After administering ADEs isolated from DIO and Lean mice to the LPS-induced ALI/ARDS model, pulmonary fibrosis degree was assessed. Then, transcriptomic analysis was performed to identify candidate molecules associated with pulmonary fibrosis, and their expression levels were detected in lung tissue samples and MLE-12 cells.

Results

LPS exposure induced severe pathological damages to lung tissue, and ADEs intervention significantly alleviated pulmonary injury induced by LPS. Transcriptomic analysis demonstrated that ADEs treatment substantially affected multiple processes of the Wnt/β-catenin/Snail pathway associated with EMT. In ALI/ARDS mouse lungs and TGF-β1-treated MLE-12 cells, ADEs administration downregulated the expression levels of Wnt3a, β-catenin, Snail and Vimentin, while upregulating the expressions of E-cadherin and p-β-catenin. Furthermore, throughout the entire experimental procedure, the anti-EMT effect of DIO-Exo outperformed that of Lean-Exo in both in vivo and in vitro settings.

Conclusions

ADEs isolated from DIO mice may potentially suppress EMT in alveolar type II epithelial cells and lung tissue in the ALI/ARDS model, possibly in association with reduced Wnt/β-catenin/Snail signalling cascade. These findings offer a promising therapeutic direction for alleviating pulmonary fibrosis associated with ALI/ARDS.