ArticleAmerican journal of respiratory cell and molecular biology2010
Endothelial-mesenchymal transition in bleomycin-induced pulmonary fibrosis.
Article in American journal of respiratory cell and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 251 papers, 1 of them a synthesis that pooled it.
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Who cites it
251 citing papers in PubMed, 1 synthesis or guideline pooled it, 453 citations in OpenAlex.
- Single cell meta-analysis of EndMT and EMT state in COVID-19.Frontiers in immunology · 2022Pooled it
- Autophagy-epithelial-mesenchymal transition crosstalk in acute respiratory distress syndrome: Mechanistic insights and therapeutic perspectives (Review).Experimental and therapeutic medicine · 2026Review
- DOT1L Drives Endothelial-to-Mesenchymal Transition and Fibrotic Vascular Remodeling via H3K79 Methylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell transcriptomics highlights macrophage-driven regulation of EndMT and repair in injured muscle.Communications biology · 2026Article
- Fibroblast activation protein inhibitor (FAPI) PET imaging in pulmonary fibrosis: pathophysiology, clinical utility, and emerging theranostic applications.Respiratory research · 2026Review
- Tweaking the Complex Fibrogenic Role of Lymphocytes in Idiopathic Pulmonary Fibrosis.Tuberculosis and respiratory diseases · 2026Article
- Integrated longitudinal transcriptomic and proteomic analysis of the murine lung response to influenza a virus.American journal of respiratory cell and molecular biology · 2026Article
- STING-STAT3-SOX18 Axis Drives EndMT and Epigenetic Reprogramming in SAVI Lung Fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Exposure of endothelial cells to doxorubicin inhibits extracellular matrix production by dermal fibroblasts in a paracrine manner.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- The Fibrotic-Cancer Continuum in IPF: Shared Mechanisms, Clinical Implications and Therapeutic Challenges.Life (Basel, Switzerland) · 2026Review
- Modulation of endothelial-to-mesenchymal transition via NRP-1 targeting with melittin attenuates pulmonary fibrosis.Materials today. Bio · 2026Article
- Pulmonary-Targeted Nanoparticles Interrupt the Malignant Mechanical and Biochemical Signaling Crosstalk for Idiopathic Pulmonary Fibrosis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Disulfiram Attenuates Bleomycin-Induced Lung Inflammation and Fibrosis with Reduced Endothelial Pyroptosis and Neutrophil Adhesion.Journal of inflammation research · 2026Article
- von Willebrand Factor: An Unhealthy Bond between Lung Endothelium and Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- IGFBP7 and CCT2 are novel lactylation-driven mediators of endothelial-to-mesenchymal transition in idiopathic pulmonary fibrosis.Functional & integrative genomics · 2025Article
- Regulation of inflammatory lung injury and repair by transforming growth factors.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Endothelial-to-mesenchymal transition in the central nervous system: A potential therapeutic target to combat age-related vascular fragility.The Journal of pharmacology and experimental therapeutics · 2025Review
- Transcription factor 4 maintains endothelial cell identity by inhibiting endothelial to mesenchymal transition.Nucleic acids research · 2025Article
- Unveiling the secret of cellular metamorphosis: the crucial role of EndMT mechanisms in COVID-19-induced pulmonary fibrosis.Inflammopharmacology · 2025Review
- The Dual Role of Perivascular Adipose Tissue in Vascular Homeostasis and Atherogenesis: From Physiology to Pathological Implications.International journal of molecular sciences · 2025Review
191 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The pathological hallmark lesions in idiopathic pulmonary fibrosis are the fibroblastic foci, in which fibroblasts are thought to be involved in the tissue remodeling, matrix deposition, and cross-talk with alveolar epithelium. Recent evidence indicates that some fibroblasts in fibrosis may be derived from bone marrow progenitors as well as from epithelial cells through epithelial-mesenchymal transition. To evaluate whether endothelial cells could represent an additional source for fibroblasts, bleomycin-induced lung fibrosis was established in Tie2-Cre/CAG-CAT-LacZ double-transgenic mice, in which LacZ was stably expressed in pan-endothelial cells. Combined X-gal staining and immunocytochemical staining for type I collagen and alpha-smooth muscle actin revealed the presence of X-gal-positive cells in lung fibroblast cultures from bleomycin-treated mice. To explore the underlying mechanisms, by which loss of endothelial-specific markers and gain of mesenchymal phenotypes could be involved in microvascular endothelial cells, the effects of activated Ras and TGF-beta on the microvascular endothelial cell line MS1 were analyzed. Combined treatment with activated Ras and TGF-beta caused a significant loss of endothelial-specific markers, while inducing de novo mesenchymal phenotypes. The altered expression of these markers in MS1 cells with activated Ras persisted after withdrawal of TGF-beta in vitro and in vivo. These findings are the first to show that lung capillary endothelial cells could give rise to significant numbers of fibroblasts through an endothelial-mesenchymal transition in bleomycin-induced lung fibrosis model.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.