ArticleInternational journal of molecular sciences2022
Cathelicidin Treatment Silences Epithelial-Mesenchymal Transition Involved in Pulmonary Fibrosis in a Murine Model of Hypersensitivity Pneumonitis.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- The Therapeutic Efficacy of Inhaled Vitamin D3 Metabolites Initiated During the Acute Phase of Hypersensitivity Pneumonitis: An In Vivo Study.Molecules (Basel, Switzerland) · 2026Article
- Vitamin D3-Deficient Diet Promotes Pulmonary Fibrosis Development in Murine Model of Hypersensitivity Pneumonitis.International journal of molecular sciences · 2025Article
- The first step for understanding the molecular mechanism of the antifibrotic effect of inhaling 25(OH)-vitamin D3 and 1,25(OH)Frontiers in pharmacology · 2025Article
- Beneficial Impact of Inhaled 25(OH)-Vitamin D3 and 1,25(OH)2-Vitamin D3 on Pulmonary Response in the Murine Model of Hypersensitivity Pneumonitis.International journal of molecular sciences · 2024Article
- FBXL8 inhibits post-myocardial infarction cardiac fibrosis by targeting Snail1 for ubiquitin-proteasome degradation.Cell death & disease · 2024Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Pulmonary fibrosis is becoming an increasingly common pathology worldwide. Unfortunately, this disorder is characterized by a bad prognosis: no treatment is known, and the survival rate is dramatically low. One of the most frequent reasons for pulmonary fibrosis is hypersensitivity pneumonitis (HP). As the main mechanism of pulmonary fibrosis is a pathology of the repair of wounded pulmonary epithelium with a pivotal role in epithelial-mesenchymal transition (EMT), we assumed that EMT silencing could prevent disease development. Because of several biological features including wound healing promotion, an ideal candidate for use in the treatment of pulmonary fibrosis seems to be cathelicidin. The aim of the studies was to understand the influence of cathelicidin on the EMT process occurring during lung fibrosis development in the course of HP. Cathelicidin's impact on EMT was examined in a murine model of HP, wherein lung fibrosis was induced by chronic exposure to extract of
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