ArticleInternational journal of molecular sciences2022
Nintedanib Inhibits Endothelial Mesenchymal Transition in Bleomycin-Induced Pulmonary Fibrosis via Focal Adhesion Kinase Activity Reduction.
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 25 papers.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- AI-driven discovery of natural product-derived FAK1 inhibitors for idiopathic pulmonary fibrosis.Molecular diversity · 2026Article
- Exploring the Molecular Mechanisms of SB216763 in the Therapeutic Intervention of Pulmonary Fibrosis Based on Macrophage Functional Plasticity.Fundamental & clinical pharmacology · 2026Article
- Piezo1 specific deletion in endothelial cell protects the progression of pulmonary fibrosis in mice.Cell communication and signaling : CCS · 2026Article
- The Relationship Between Differential Expression of Non-coding RNAs (TP53TG1, LINC00342, MALAT1, DNM3OS, miR-126-3p, miR-200a-3p, miR-18a-5p) and Protein-Coding Genes (PTEN, FOXO3) and Risk of Idiopathic Pulmonary Fibrosis.Biochemical genetics · 2026Article
- The Endothelial Cell Perspective in Pulmonary Fibrosis: From Cell Fate Decisions, Intercellular Communication, and EndoMT to Emerging Therapies.Canadian respiratory journal · 2026Review
- Endothelial-to-Mesenchymal Transition in Health and Disease: Molecular Insights and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Biofabrication of a 3D human skeletal muscle microenvironment to study the early steps of fibrosis.Materials today. Bio · 2025Article
- IGFBP7 and CCT2 are novel lactylation-driven mediators of endothelial-to-mesenchymal transition in idiopathic pulmonary fibrosis.Functional & integrative genomics · 2025Article
- PDE4-Selective Inhibition in Chronic Obstructive Pulmonary Disease and Pulmonary Fibrosis: Different Agents or Different Targets?Life (Basel, Switzerland) · 2025Review
- Antifibrotic Efficacy of a Nintedanib-Peptide Conjugate and Diagnostic Potential of a Fluorescent Companion Probe Targeting αACS pharmacology & translational science · 2025Article
- Analysis of the therapeutic effect and potential mechanism of FeMaterials today. Bio · 2025Article
- Quantification and Analysis of Lung Involvement by Artificial Intelligence in Patients with Progressive Pulmonary Fibrosis Treated with Nintedanib.Medicina (Kaunas, Lithuania) · 2025Article
- Clinical relevance of microvascular endothelial dysfunction in idiopathic pulmonary fibrosis.ERJ open research · 2025Article
- MDA5 protein mediating persistent ER stress/unfolded protein response contributes to endothelial-mesenchymal-transition of lung microvascular endothelial cell in dermatomyositis.Cell communication and signaling : CCS · 2025Article
- Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition.Cell communication and signaling : CCS · 2025Review
- GTX-11 attenuates lung fibrosis, inflammation and vascular remodeling in preclinical models of lung fibrotic disease.Frontiers in pharmacology · 2025Article
- Vascular involvement in idiopathic pulmonary fibrosis.ERJ open research · 2024Review
- Multicenter, prospective, observational study for urinary exosomal biomarkers of kidney allograft fibrosis.Scientific reports · 2024Observational
- Current state of signaling pathways associated with the pathogenesis of idiopathic pulmonary fibrosis.Respiratory research · 2024Review
- Exosomes derived from adipose tissue-derived stem cells alleviated HCell biology and toxicology · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease (ILD). Pulmonary fibroblasts play an important role in the development of IPF. Emerging evidence indicates that pulmonary endothelial cells could be the source of pulmonary fibroblasts through endothelial mesenchymal transition (EndoMT), which contributes to pulmonary fibrosis. EndoMT is a complex process in which endothelial cells lose their expression of endothelial markers and give rise to the characteristics of mesenchymal cells, including morphological fibroblast-like change and the expression of mesenchymal markers, which result in cardiac, renal, and dermal fibroses. Furthermore, EndoMT inhibition attenuates pulmonary fibrosis. Herein, we demonstrate that nintedanib, a tyrosine kinase receptor inhibitor, ameliorated murine bleomycin (BLM)-induced pulmonary fibrosis and suppressed the in vivo and in vitro models of EndoMT. We demonstrated that the activity of focal adhesion kinase (FAK), a key EndoMT regulator, increased in murine lung tissues and human pulmonary microvascular endothelial cells after BLM stimulation. Nintedanib treatment inhibited BLM-induced FAK activation and thus suppressed both in vivo and in vitro BLM-induced EndoMT. Importantly, we found that the VEGF/FAK signaling pathway was involved in nintedanib regulating EndoMT. These novel findings help us understand the mechanism and signaling pathway of EndoMT to further develop more efficacious drugs for IPF treatment.
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