ArticlePulmonary circulation2011
Oxidative injury is a common consequence of BMPR2 mutations.
Article in Pulmonary circulation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- Cellular Signalling Networks in High Altitude Pulmonary Hypertension: From Canonical Pathways to Emerging Targets.Cell proliferation · 2026Review
- Alterations in Mitochondrial Function in Pulmonary Vascular Diseases.Antioxidants & redox signaling · 2025Article
- Article
- Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension.Biomedicines · 2022Review
- An Overview of Circulating Pulmonary Arterial Hypertension Biomarkers.Frontiers in cardiovascular medicine · 2022Review
- Sex Dimorphism in Pulmonary Hypertension: The Role of the Sex Chromosomes.Antioxidants (Basel, Switzerland) · 2021Review
- Article
- Potential role of cartilage oligomeric matrix protein in the modulation of pulmonary arterial smooth muscle superoxide by hypoxia.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Oxidative stress increases M1dG, a major peroxidation-derived DNA adduct, in mitochondrial DNA.Nucleic acids research · 2018Article
- Bone morphogenetic protein signaling is required for RAD51-mediated maintenance of genome integrity in vascular endothelial cells.Communications biology · 2018Article
- Oestrogen inhibition reverses pulmonary arterial hypertension and associated metabolic defects.The European respiratory journal · 2017Article
- Reactive Oxygen and Nitrogen Species in the Development of Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2017Review
- Dysfunctional BMPR2 signaling drives an abnormal endothelial requirement for glutamine in pulmonary arterial hypertension.Pulmonary circulation · 2017Article
- Role of oxidized lipids in pulmonary arterial hypertension.Pulmonary circulation · 2016Review
- Antagonism of the thromboxane-prostanoid receptor is cardioprotective against right ventricular pressure overload.Pulmonary circulation · 2016Article
- Accumulation of isolevuglandin-modified protein in normal and fibrotic lung.Scientific reports · 2016Article
- Article
- Redox biology in pulmonary arterial hypertension (2013 Grover Conference Series).Pulmonary circulation · 2015Review
- Expression of mutant bone morphogenetic protein receptor II worsens pulmonary hypertension secondary to pulmonary fibrosis.Pulmonary circulation · 2015Article
- Bone morphogenetic protein receptor type II deficiency and increased inflammatory cytokine production. A gateway to pulmonary arterial hypertension.American journal of respiratory and critical care medicine · 2015Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHereditary pulmonary arterial hypertension(PAH) is usually caused by mutations in BMPR2. Mutations are found throughout the gene, and common molecular consequences of different types of mutation are not known. Knowledge of common molecular consequences would provide insight into molecular etiology of disease. The objective of this study was to determine common molecular consequences across classes of BMPR2 mutation. METHODS #ENTITYSTARTX00026;
resultsIncreased superoxide and peroxide production, and alterations in genes associated with oxidative stress were a common consequence of stable transfection of vascular smooth muscle cells with three distinct classes of BMPR2 mutation, in the ligand binding domain, the kinase domain, and the cytoplasmic tail domain. Measurement of oxidized lipids in whole lung from transgenic mice expressing a mutation in the BMPR2 cytoplasmic tail showed a 50% increase in isoprostanes and a twofold increase in isofurans, suggesting increased ROS of mitochondrial origin. Immunohistochemistry on BMPR2 transgenic mouse lung showed that oxidative stress was vascular-specific. Electron microscopy showed decreased mitochondrial size and variability in pulmonary vessels from BMPR2 mutant mice. Measurement of oxidized lipids in urine from humans with BMPR2 mutations demonstrated increased ROS, regardless of disease status. Immunohistochemistry on HPAH patient lung confirmed oxidative stress specific to the vasculature.
conclusionsIncreased oxidative stress, likely of mitochondrial origin, is a common consequence of BMPR2 mutation across mutation types in cell culture, mice, and humans.
Identifiers
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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.