ArticlePulmonary circulation2015
Expression of mutant bone morphogenetic protein receptor II worsens pulmonary hypertension secondary to pulmonary fibrosis.
Article in Pulmonary circulation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The trial behind it
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Nedd4L-mediated stabilization of morphogenetic protein receptor 2 in lung fibroblasts confers protection against pulmonary fibrosis.Signal transduction and targeted therapy · 2026Article
- von Willebrand Factor: An Unhealthy Bond between Lung Endothelium and Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- Inhibition of BMPER Mitigates Pulmonary Hypertension by Modulating LRP1-YAP Interaction in Smooth Muscle Cells.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Emerging role of BMPs/BMPR2 signaling pathway in treatment for pulmonary fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Review
- Repetitive sulfur dioxide exposure in mice models post-deployment respiratory syndrome.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Pharmacology and Emerging Therapies for Group 3 Pulmonary Hypertension Due to Chronic Lung Disease.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Metabolism in Pulmonary Hypertension.Annual review of physiology · 2021Review
- Volume Load-Induced Right Ventricular Failure in Rats Is Not Associated With Myocardial Fibrosis.Frontiers in physiology · 2021Article
- Emergency myelopoiesis contributes to immune cell exhaustion and pulmonary vascular remodelling.British journal of pharmacology · 2021Article
- Expression of a Human Caveolin-1 Mutation in Mice Drives Inflammatory and Metabolic Defect-Associated Pulmonary Arterial Hypertension.Frontiers in medicine · 2020Article
- Chemokine signaling axis between endothelial and myeloid cells regulates development of pulmonary hypertension associated with pulmonary fibrosis and hypoxia.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Inflammatory Macrophage Expansion in Pulmonary Hypertension Depends upon Mobilization of Blood-Borne Monocytes.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Myeloid-derived Suppressor Cells Are Necessary for Development of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2018Article
- rhACE2 Therapy Modifies Bleomycin-Induced Pulmonary Hypertension via Rescue of Vascular Remodeling.Frontiers in physiology · 2018Article
- Vascular Endothelial Cell-Specific Connective Tissue Growth Factor (CTGF) Is Necessary for Development of Chronic Hypoxia-Induced Pulmonary Hypertension.Frontiers in physiology · 2018Article
- Origin and production of inflammatory perivascular macrophages in pulmonary hypertension.Cytokine · 2017Review
- BMPR2 and HIF1-Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2017Article
- Disruption of lineage specification in adult pulmonary mesenchymal progenitor cells promotes microvascular dysfunction.The Journal of clinical investigation · 2017Article
- Pulmonary Hypertension Associated with Idiopathic Pulmonary Fibrosis: Current and Future Perspectives.Canadian respiratory journal · 2017Review
- The Action of Smooth Muscle Cell Potassium Channels in the Pathology of Pulmonary Arterial Hypertension.Pediatric cardiology · 2017Review
Corrections and comments
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Authors and funding
18 authors at 2 institutions in 1 country.
Funding
Abstract
Pulmonary fibrosis is often complicated by pulmonary hypertension (PH), and previous studies have shown a potential link between bone morphogenetic protein receptor II (BMPR2) and PH secondary to pulmonary fibrosis. We exposed transgenic mice expressing mutant BMPR2 and control mice to repetitive intraperitoneal injections of bleomycin for 4 weeks. The duration of transgene activation was too short for mutant BMPR2 mice to develop spontaneous PH. Mutant BMPR2 mice had increased right ventricular systolic pressure compared to control mice, without differences in pulmonary fibrosis. We found increased hypoxia-inducible factor (HIF)1-α stabilization in lungs of mutant-BMPR2-expressing mice compared to controls following bleomycin treatment. In addition, expression of the hypoxia response element protein connective tissue growth factor was increased in transgenic mice as well as in a human pulmonary microvascular endothelial cell line expressing mutant BMPR2. In mouse pulmonary vascular endothelial cells, mutant BMPR2 expression resulted in increased HIF1-α and reactive oxygen species production following exposure to hypoxia, both of which were attenuated with the antioxidant TEMPOL. These data suggest that expression of mutant BMPR2 worsens secondary PH through increased HIF activity in vascular endothelium. This pathway could be therapeutically targeted in patients with PH secondary to pulmonary fibrosis.
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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.