ArticleArteriosclerosis, thrombosis, and vascular biology2015
Genetic Ablation of PDGF-Dependent Signaling Pathways Abolishes Vascular Remodeling and Experimental Pulmonary Hypertension.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- The Role of Platelets in Pulmonary Hypertension: From Activation to Pulmonary Vascular Remodeling-A Review Article.Biomedicines · 2026Review
- METTL3 mediates mJournal of advanced research · 2026Article
- Exploring the Impact of Platelet-Derived Growth Factor D in Pulmonary Hypertension Development.Pulmonary circulation · 2025Article
- Novel Insights Into Receptor Tyrosine Kinases in Pulmonary Arterial Hypertension.Journal of the American Heart Association · 2025Review
- Growth factors involved in vascular remodeling in pulmonary arterial hypertension.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2025Review
- C-type natriuretic peptide/cGMP/FoxO3 signaling attenuates hyperproliferation of pericytes from patients with pulmonary arterial hypertension.Communications biology · 2024Article
- IMPAHCT: A randomized phase 2b/3 study of inhaled imatinib for pulmonary arterial hypertension.Pulmonary circulation · 2024Article
- Pharmacology and Rationale for Seralutinib in the Treatment of Pulmonary Arterial Hypertension.International journal of molecular sciences · 2023Review
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Vascular pathobiology of pulmonary hypertension.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2023Review
- The Provenance, Providence, and Position of Endothelial Cells in Injured Spinal Cord Vascular Pathology.Cellular and molecular neurobiology · 2023Review
- Inhaled seralutinib exhibits potent efficacy in models of pulmonary arterial hypertension.The European respiratory journal · 2022Article
- The Platelet-Derived Growth Factor Pathway in Pulmonary Arterial Hypertension: Still an Interesting Target?Life (Basel, Switzerland) · 2022Review
- Platelet-Derived Growth Factor Receptor Type α Activation Drives Pulmonary Vascular Remodeling Via Progenitor Cell Proliferation and Induces Pulmonary Hypertension.Journal of the American Heart Association · 2022Article
- TRPC6, a therapeutic target for pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Disrupted PI3K subunit p110α signaling protects against pulmonary hypertension and reverses established disease in rodents.The Journal of clinical investigation · 2021Article
- Review
- Macrophage-derived PDGF-B induces muscularization in murine and human pulmonary hypertension.JCI insight · 2021Article
- mTOR Signaling in Pulmonary Vascular Disease: Pathogenic Role and Therapeutic Target.International journal of molecular sciences · 2021Review
- Single-Cell Transcriptomics Reveals the Cellular Heterogeneity of Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveDespite modern therapies, pulmonary arterial hypertension (PAH) harbors a high mortality. Vascular remodeling is a hallmark of the disease. Recent clinical studies revealed that antiremodeling approaches with tyrosine-kinase inhibitors such as imatinib are effective, but its applicability is limited by significant side effects. Although imatinib has multiple targets, expression analyses support a role for platelet-derived growth factor (PDGF) in the pathobiology of the disease. However, its precise role and downstream signaling events have not been established. APPROACH AND
resultsPatients with PAH exhibit enhanced expression and phosphorylation of β PDGF receptor (βPDGFR) in remodeled pulmonary arterioles, particularly at the binding sites for phophatidyl-inositol-3-kinase and PLCγ at tyrosine residues 751 and 1021, respectively. These signaling molecules were identified as critical downstream mediators of βPDGFR-mediated proliferation and migration of pulmonary arterial smooth muscle cells. We, therefore, investigated mice expressing a mutated βPDGFR that is unable to recruit phophatidyl-inositol-3-kinase and PLCγ (βPDGFR(F3/F3)). PDGF-dependent Erk1/2 and Akt phosphorylation, cyclin D1 induction, and proliferation, migration, and protection against apoptosis were abolished in βPDGFR(F3/F3) pulmonary arterial smooth muscle cells. On exposure to chronic hypoxia, vascular remodeling of pulmonary arteries was blunted in βPDGFR(F3/F3) mice compared with wild-type littermates. These alterations led to protection from hypoxia-induced PAH and right ventricular hypertrophy.
conclusionsBy means of a genetic approach, our data provide definite evidence that the activated βPDGFR is a key contributor to pulmonary vascular remodeling and PAH. Selective disruption of PDGF-dependent phophatidyl-inositol-3-kinase and PLCγ activity is sufficient to abolish these pathogenic responses in vivo, identifying these signaling events as valuable targets for antiremodeling strategies in PAH.
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