ArticleTobacco induced diseases2025
Smad7 ameliorate small airway remodeling in COPD by modulating epithelial-mesenchymal transition.
Article in Tobacco induced diseases, 2025. 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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Who cites it
1 citing paper in PubMed.
- Epithelial cells in chronic obstructive pulmonary disease exacerbations: Targets for lung repair.Pharmacological reviews · 2026Review
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4 authors.
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Abstract
introductionSmall airway remodeling is a key pathological feature of COPD, yet its mechanisms remain unclear. TGF-β1 induces epithelial-mesenchymal transition (EMT), contributing to airway remodeling. Smad7 is a negative regulator of TGF-β signaling, but its role in COPD remains undefined. This study investigates whether Smad7 suppresses TGF-β1-induced EMT in COPD small airway remodeling.
methodsLung tissues from COPD patients (n=3 for each group) and mouse models (n=5 for each group) were analyzed for EMT markers and collagen deposition. BEAS-2B cells were exposed to cigarette smoke extract (CSE) to assess TGF-β1 secretion. EMT markers (E-Cadherin, N-Cadherin, and Vimentin) were evaluated using RT-qPCR, Western blot, and immunofluorescence staining. Morphological changes were examined, and Smad7 function was assessed via overexpression and knockdown experiments.
resultsCOPD patients and mouse models showed increased EMT and collagen deposition. CSE exposure upregulated TGF-β1 in BEAS-2B cells, leading to decreased E-Cadherin and increased N-Cadherin and Vimentin. Morphological changes confirmed EMT induction. Overexpression of Smad7 reversed these effects, while its knockdown enhanced them.
conclusionsSmoking promotes TGF-β1-induced small airway remodeling in COPD by driving EMT. Smad7 suppresses this process.
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