ArticleCirculation2005
Increased susceptibility to pulmonary hypertension in heterozygous BMPR2-mutant mice.
Article in Circulation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 205 citations in OpenAlex.
- A rare recurring gain-of-function variant in BMPR2 causes neurodevelopmental phenotypes in humans and flies.American journal of human genetics · 2026Article
- Harnessing NLRX1: a new frontier in mitigating inflammation in pulmonary hypertension.Respiratory research · 2025Article
- Experimental animal models and patient-derived platforms to bridge preclinical discovery and translational therapeutics in pulmonary arterial hypertension.Journal of translational medicine · 2025Review
- ATP13A3 variants promote pulmonary arterial hypertension by disrupting polyamine transport.Cardiovascular research · 2024Article
- Reversal of Pulmonary Hypertension in a Human-Like Model: Therapeutic Targeting of Endothelial DHFR.Circulation research · 2024Article
- Defining the clinical validity of genes reported to cause pulmonary arterial hypertension.Genetics in medicine : official journal of the American College of Medical Genetics · 2023Article
- Inactivating the Uninhibited: The Tale of Activins and Inhibins in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2023Review
- Bmpr2 mutant mice are an inadequate model for studying iron deficiency in pulmonary hypertension.Pulmonary circulation · 2022Article
- The Latest in Animal Models of Pulmonary Hypertension and Right Ventricular Failure.Circulation research · 2022Review
- New Mutations and Pathogenesis of Pulmonary Hypertension: Progress and Puzzles in Disease Pathogenesis.Circulation research · 2022Review
- Pulmonary Arterial Hypertension: Emerging Principles of Precision Medicine across Basic Science to Clinical Practice.Reviews in cardiovascular medicine · 2022Article
- Approaches to treat pulmonary arterial hypertension by targeting BMPR2: from cell membrane to nucleus.Cardiovascular research · 2021Review
- Developmental programming of DNA methylation and gene expression patterns is associated with extreme cardiovascular tolerance to anoxia in the common snapping turtle.Epigenetics & chromatin · 2021Article
- Improving Right Ventricular Function by Increasing BMP Signaling with FK506.American journal of respiratory cell and molecular biology · 2021Article
- Therapeutic Approaches for Treating Pulmonary Arterial Hypertension by Correcting Imbalanced TGF-β Superfamily Signaling.Frontiers in medicine · 2021Review
- 'There and Back Again'-Forward Genetics and Reverse Phenotyping in Pulmonary Arterial Hypertension.Genes · 2020Review
- EndothelialArteriosclerosis, thrombosis, and vascular biology · 2020Article
- The integrated stress response in pulmonary disease.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Formulation and Characterization of Solid Lipid Nanoparticles Loading RF22-c, a Potent and Selective 5-LO Inhibitor, in a Monocrotaline-Induced Model of Pulmonary Hypertension.Frontiers in pharmacology · 2020Article
- Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundBone morphogenetic protein receptor-2 (BMPR2)-heterozygous, mutant (BMPR2(+/-)) mice have a genetic trait similar to that of certain patients with idiopathic pulmonary arterial hypertension (IPAH). To understand the role of BMPR2 in the development of IPAH, we examined the phenotype of BMPR2(+/-) mice and their response to inflammatory stress. METHODS AND
resultsBMPR2(+/-) mice were found to have the same life span, right ventricular systolic pressure (RVSP), and lung histology as those of wild-type mice under unstressed conditions. However, when treated with recombinant adenovirus expressing 5-lipoxygenase (Ad5LO), BMPR2(+/-) mice exhibited significantly higher RVSP than wild-type mice. The increase of RVSP occurred in the first 2 weeks after Ad5LO delivery. Modest but significant muscularization of distal pulmonary arterioles appeared in BMPR2(+/-) mice 4 weeks after Ad5LO treatment. Measurement of urinary metabolites of vasoactive molecules showed that cysteinyl leukotrienes, prostacyclin metabolites, and PGE2 were all increased to a similar degree in both BMPR2(+/-) and wild-type mice during 5LO transgene expression, whereas urinary endothelin-1 remained undetectable. Urinary thromboxane A2 metabolites, in contrast, were significantly higher in BMPR2(+/-) than in wild-type mice and paralleled the increase in RVSP. Platelet activation markers, serotonin, and soluble P-selectin showed a trend toward higher concentrations in BMPR2(+/-) than wild-type mice. Cell culture studies found that BMP treatment reduced interleukin-1beta-stimulated thromboxane A2 production in the pulmonary epithelial cell line A549.
conclusionsBMPR2(+/-) mice do not develop pulmonary hypertension spontaneously; however, under inflammatory stress, they are more susceptible to an increase in RVSP, thromboxane A2 production, and vascular remodeling than wild-type mice.
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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.