ArticleAmerican journal of respiratory cell and molecular biology2013
Endothelial cells recruit macrophages and contribute to a fibrotic milieu in bleomycin lung injury.
Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 80 citations in OpenAlex.
- Physical exercise in patients with testicular cancer treated with bleomycin, etoposide and cisplatin chemotherapy: pulmonary and vascular endothelial function-an exploratory analysis.Journal of cancer research and clinical oncology · 2023Trial
- Yohimbine attenuates bleomycin-induced skin fibrosis by modulating the PI3K/Akt-MAPK signaling: an integrated network pharmacology and in vivo study.Journal of molecular histology · 2026Article
- Review
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- von Willebrand Factor Deficiency Inhibits Endothelial-to-Mesenchymal Transition to Attenuate Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- Prognostic value of pulmonary vessel-related structures in rapid progression of idiopathic inflammatory myopathy-associated interstitial lung disease: a retrospective study from two centres.BMJ open respiratory research · 2025Article
- The LPAR1 antagonist, PIPE-791 produces antifibrotic effects in models of lung fibrosis.Respiratory research · 2025Article
- Human Tendon-on-a-Chip for Modeling the Myofibroblast Microenvironment in Peritendinous Fibrosis.Advanced healthcare materials · 2025Article
- The role of vascularity and the fibrovascular interface in interstitial lung diseases.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025Review
- Development of immunocompetent full thickness skin tissue constructs to model skin fibrosis for high-throughput drug screening.Biofabrication · 2024Article
- Development of a machine learning model in prediction of the rapid progression of interstitial lung disease in patients with idiopathic inflammatory myopathy.Quantitative imaging in medicine and surgery · 2024Article
- The role of vasculature and angiogenesis in respiratory diseases.Angiogenesis · 2024Review
- Roles of Macrophages and Endothelial Cells and Their Crosstalk in Acute Lung Injury.Biomedicines · 2024Review
- Single-Cell Transcriptomic Analysis of Salivary Gland Endothelial Cells.Journal of dental research · 2024Article
- Fibroblasts and endothelial cells interplay drives hypertrophic scar formation: Insights from in vitro and in vivo models.Bioengineering & translational medicine · 2024Article
- Human tendon-on-a-chip for modeling vascular inflammatory fibrosis.Research square · 2023Article
- Monoclonal enolase-1 blocking antibody ameliorates pulmonary inflammation and fibrosis.Respiratory research · 2023Article
- The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023Review
- A Protective Effect of Pirfenidone in Lung Fibroblast-Endothelial Cell Network via Inhibition of Rho-Kinase Activity.Biomedicines · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Systemic sclerosis (SSc) is a systemic autoimmune disease that causes inflammation, vasculopathy, and fibrosis of the skin and internal organs. One of the most severe complications of SSc involves the development of pulmonary fibrosis. Endothelial cell injury precedes the development of fibrosis, and is believed to be an initiating event. Therefore, we aimed to characterize the role of endothelial cells in the progression of pulmonary fibrosis, using a well-established bleomycin (BLM) model of pulmonary fibrosis. Endothelial cells were isolated by cell sorting, and the analysis of gene expression was performed with quantitative RT-PCR. Endothelial injury was induced between the first and second week, as shown by the elevated expression of the vascular injury markers matrix metallopeptidase-12 and von Willebrand factor. After injury, endothelial activation was indicated by the up-regulation of selectins, CCL chemokines, and inflammatory mediators, including complement anaphylatoxin receptors (C3aR and C5aR), oncostatin M, and leukemia inhibitory factor. The endothelial cell overexpression of fibrotic mediators, including connective tissue growth factor, plasminogen activator inhibitor-1, osteopontin, fibronectin, and fibroblast specific protein-1, was observed in the second and fourth weeks. This study suggests that endothelial cells actively contribute to the disease process via multiple mechanisms, including the recruitment of inflammatory cells and the establishment of a profibrotic environment during the development of BLM-induced pulmonary fibrosis.
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