ArticleJournal of translational medicine2026
Adipose-derived exosomes alleviate ALI via inhibiting epithelial-mesenchymal transition of alveolar type II cells by Wnt/β-catenin/snail pathway.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Pharmacological modulation of cGAS-STING-NLRP3 signaling by nano-immunomodulators in Alzheimer and Parkinson disease.Inflammopharmacology · 2026Review
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9 authors.
Funding
Abstract
backgroundAcute 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.
methodsAfter 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.
resultsLPS 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.
conclusionsADEs 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.
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