ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Macrophage bone morphogenic protein receptor 2 depletion in idiopathic pulmonary fibrosis and Group III pulmonary hypertension.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 80 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
- Navigating the Complexity of PH-ILD: From Molecular Mechanisms to Integrated Clinical Evaluation.International journal of molecular sciences · 2026Review
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- Review of the Diagnosis and Management of Pulmonary Hypertension Associated with Interstitial Lung Disease (ILD-PH).Journal of clinical medicine · 2025Review
- Vascular involvement in idiopathic pulmonary fibrosis.ERJ open research · 2024Review
- Dissecting the lung transcriptome of pulmonary fibrosis-associated pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Converging Pathways: A Review of Pulmonary Hypertension in Interstitial Lung Disease.Life (Basel, Switzerland) · 2024Review
- Emerging role of BMPs/BMPR2 signaling pathway in treatment for pulmonary fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Review
- BMP2 Diminishes Angiotensin II-Induced Atrial Fibrillation by Inhibiting NLRP3 Inflammasome Signaling in Atrial Fibroblasts.Biomolecules · 2024Article
- Epithelium-derived exosomes promote silica nanoparticles-induced pulmonary fibroblast activation and collagen deposition via modulating fibrotic signaling pathways and their epigenetic regulations.Journal of nanobiotechnology · 2024Article
- Future Perspectives of Pulmonary Arterial Hypertension: A Review of Novel Pipeline Treatments and Indications.Drugs in R&D · 2024Review
- The role of IL-6/JAK/STAT signal in female infertility caused by hydrosalpinx.Immunity, inflammation and disease · 2023Article
- Lipid nanoparticle-mediated mRNA delivery in lung fibrosis.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2023Article
- Review
- Pharmacology and Emerging Therapies for Group 3 Pulmonary Hypertension Due to Chronic Lung Disease.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Tensions in Taxonomies: Current Understanding and Future Directions in the Pathobiologic Basis and Treatment of Group 1 and Group 3 Pulmonary Hypertension.Comprehensive Physiology · 2023Review
- Identification of the shared gene signatures between pulmonary fibrosis and pulmonary hypertension using bioinformatics analysis.Frontiers in immunology · 2023Article
- Bone morphogenetic protein 4 inhibits pulmonary fibrosis by modulating cellular senescence and mitophagy in lung fibroblasts.The European respiratory journal · 2022Article
- E2F1 regulates miR-215-5p to aggravate paraquat-induced pulmonary fibrosis via repressing BMPR2 expression.Toxicology research · 2022Article
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Authors and funding
20 authors at 5 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease of unknown etiology. The development of pulmonary hypertension (PH) is considered the single most significant predictor of mortality in patients with chronic lung diseases. The processes that govern the progression and development of fibroproliferative and vascular lesions in IPF are not fully understood. Using human lung explant samples from patients with IPF with or without a diagnosis of PH as well as normal control tissue, we report reduced BMPR2 expression in patients with IPF or IPF+PH. These changes were consistent with dampened P-SMAD 1/5/8 and elevated P-SMAD 2/3, demonstrating reduced BMPR2 signaling and elevated TGF-β activity in IPF. In the bleomycin (BLM) model of lung fibrosis and PH, we also report decreased BMPR2 expression compared with control animals that correlated with vascular remodeling and PH. We show that genetic abrogation or pharmacological inhibition of interleukin-6 leads to diminished markers of fibrosis and PH consistent with elevated levels of BMPR2 and reduced levels of a collection of microRNAs (miRs) that are able to degrade BMPR2. We also demonstrate that isolated bone marrow-derived macrophages from BLM-exposed mice show reduced BMPR2 levels upon exposure with IL6 or the IL6+IL6R complex that are consistent with immunohistochemistry showing reduced BMPR2 in CD206 expressing macrophages from lung sections from IPF and IPF+PH patients. In conclusion, our data suggest that depletion of BMPR2 mediated by a collection of miRs induced by IL6 and subsequent STAT3 phosphorylation as a novel mechanism participating to fibroproliferative and vascular injuries in IPF.
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