ArticleJournal of cellular and molecular medicine2025
Cinobufotalin Ameliorates the Development of Pulmonary Fibrosis by Suppressing the TGF-β/Smad Pathway via Regulating PI15.
Article in Journal of cellular and molecular medicine, 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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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
1 citing paper in PubMed.
- Cinobufotalin Ameliorates the Development of Pulmonary Fibrosis by Suppressing the TGF-β/Smad Pathway via Regulating PI15.Journal of cellular and molecular medicine · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Pulmonary fibrosis (PF) is a common hallmark of several types of interstitial lung diseases (ILDs), for which effective therapeutic drugs are lacking. The small-molecule chemical compound cinobufotalin (CB) has demonstrated significant anti-cancer effects in lung cancer. In this study, we first found that CB attenuated bleomycin (BLM)-induced PF and inhibited transforming growth factor-beta 1 (TGF-β1)-induced myofibroblast activation and epithelial-mesenchymal transition (EMT). Subsequently, comparative RNA sequencing (RNA-Seq) was conducted to analyse the lung gene expression profiles in mice. Interestingly, peptidase inhibitor 15 (PI15) was identified as a significantly differentially expressed gene (DEG) and may be a potential target in PF progression. Mechanistic studies showed that CB exerts anti-PF effects by inhibiting PI15 and thereby regulating the TGF-β/Smad signalling pathway. Our data demonstrated that CB represents a promising anti-PF drug and may be a candidate therapeutic for PF patients.
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