ArticleActa pharmaceutica Sinica. B2024
Ailanthone ameliorates pulmonary fibrosis by suppressing JUN-dependent MEOX1 activation.
Article in Acta pharmaceutica Sinica. B, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Targeting NOX4 with Quercetagetin-PLGA nanomaterials: a novel therapeutic strategy for Alzheimer's disease.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- MEOX1 Inhibits Growth and Metastasis of Salivary Adenoid Cystic Carcinoma.Current issues in molecular biology · 2026Article
- γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response.Nature communications · 2026Article
- Transferosomes as Advanced Nanocarriers for Enhanced Drug Delivery in Skin Cancer Therapy: A Comprehensive Review.Applied biochemistry and biotechnology · 2026Review
- Target discovery-directed pharmacological mechanism elucidation of bioactive natural products.Medical review (2021) · 2025Review
- SRSF7 promotes pulmonary fibrosis through regulating PKM alternative splicing in lung fibroblasts.Acta pharmaceutica Sinica. B · 2025Article
- The crucial function of IDO1 in pulmonary fibrosis: From the perspective of mitochondrial fusion in lung fibroblasts and targeted molecular inhibition.Acta pharmaceutica Sinica. B · 2025Article
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Authors and funding
15 authors.
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Abstract
Pulmonary fibrosis poses a significant health threat with very limited therapeutic options available. In this study, we reported the enhanced expression of mesenchymal homobox 1 (MEOX1) in pulmonary fibrosis patients, especially in their fibroblasts and endothelial cells, and confirmed MEOX1 as a central orchestrator in the activation of profibrotic genes. By high-throughput screening, we identified Ailanthone (AIL) from a natural compound library as the first small molecule capable of directly targeting and suppressing MEOX1. AIL demonstrated the ability to inhibit both the activation of fibroblasts and endothelial-to-mesenchymal transition of endothelial cells when challenged by transforming growth factor-
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