ArticleThe Journal of clinical investigation2009
Endothelial-derived FGF2 contributes to the progression of pulmonary hypertension in humans and rodents.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
100 citing papers in PubMed, 209 citations in OpenAlex.
- Treprostinil increases the number and angiogenic potential of endothelial progenitor cells in children with pulmonary hypertension.Angiogenesis · 2011Trial
- FGF family in health and disease.Molecular biomedicine · 2026Review
- 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
- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- Molecular Pathogenesis of Connective Tissue Disease-Associated Pulmonary Arterial Hypertension: A Narrative Review.Biomolecules · 2025Review
- Morphometric and Molecular Interplay in Hypertension-Induced Cardiac Remodeling with an Emphasis on the Potential Therapeutic Implications.International journal of molecular sciences · 2025Review
- FGF2 is secreted in extracellular vesicles from lung cells.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- The role of p130Cas/BCAR1 adaptor protein in the pathogenesis of cardiovascular diseases: A literature review.American heart journal plus : cardiology research and practice · 2024Review
- Endothelial HIFα/PDGF-B to smooth muscle Beclin1 signaling sustains pathological muscularization in pulmonary hypertension.JCI insight · 2024Article
- Exploring the pathogenesis of pulmonary vascular disease.Frontiers in medicine · 2024Review
- The Effect of Hypoxia-inducible Factor Inhibition on the Phenotype of Fibroblasts in Human and Bovine Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2023Article
- An emerging class of new therapeutics targeting TGF, Activin, and BMP ligands in pulmonary arterial hypertension.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Review
- Pathophysiology and new advances in pulmonary hypertension.BMJ medicine · 2023Review
- Lymphoedema conditions disrupt endothelial barrier functionJournal of the Royal Society, Interface · 2022Article
- Periostin-related progression of different types of experimental pulmonary hypertension: A role for M2 macrophage and FGF-2 signalling.Respirology (Carlton, Vic.) · 2022Article
- 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
- Review
- Effects of FW2 Nanoparticles Toxicity in a New In Vitro Pulmonary Vascular Cells Model Mimicking Endothelial Dysfunction.Cardiovascular toxicology · 2022Article
- Hepatoma-derived growth factor is associated with pulmonary vascular remodeling and PAH disease severity and survival.Pulmonary circulation · 2022Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary hypertension (PH) is a progressive, lethal lung disease characterized by pulmonary artery SMC (PA-SMC) hyperplasia leading to right-sided heart failure. Molecular events originating in pulmonary ECs (P-ECs) may contribute to the PA-SMC hyperplasia in PH. Thus, we exposed cultured human PA-SMC to medium conditioned by P-EC from patients with idiopathic PH (IPH) or controls and found that IPH P-EC-conditioned medium increased PA-SMC proliferation more than control P-EC medium. Levels of FGF2 were increased in the medium of IPH P-ECs over controls, while there was no detectable difference in TGF-beta1, PDGF-BB, or EGF levels. No difference in FGF2-induced proliferation or FGF receptor type 1 (FGFR1) mRNA levels was detected between IPH and control PA-SMCs. Knockdown of FGF2 in P-EC using siRNA reduced the PA-SMC growth-stimulating effects of IPH P-EC medium by 60% and control P-EC medium by 10%. In situ hybridization showed FGF2 overproduction predominantly in the remodeled vascular endothelium of lungs from patients with IPH. Repeated intravenous FGF2-siRNA administration abolished lung FGF2 production, both preventing and nearly reversing a rat model of PH. Similarly, pharmacological FGFR1 inhibition with SU5402 reversed established PH in the same model. Thus, endothelial FGF2 is overproduced in IPH and contributes to SMC hyperplasia in IPH, identifying FGF2 as a promising target for new treatments against PH.
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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.