ArticlePulmonary circulation2016
Antagonism of the thromboxane-prostanoid receptor is cardioprotective against right ventricular pressure overload.
Article in Pulmonary circulation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- Structural and dynamic insights into agonist recognition and function of the thromboxane ANature communications · 2026Article
- Targeting platelet-tumor cell interactions via thromboxane AExperimental hematology & oncology · 2025Article
- Emerging therapies for the treatment of systemic sclerosis.Nature reviews. Rheumatology · 2025Review
- Association of Systemic Thromboxane Generation With Risk of Developing Heart Failure.Journal of the American College of Cardiology · 2025Article
- Blockade of thromboxane A2 signaling attenuates ethanol-induced myocardial inflammatory response in mice.Alcohol, clinical & experimental research · 2024Article
- Adjustment for Renal Function Improves the Prognostic Performance of Urinary Thromboxane Metabolites.Clinical chemistry · 2024Article
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Evaluation ofFrontiers in pharmacology · 2023Article
- Thromboxane-Prostanoid Receptor Signaling Drives Persistent Fibroblast Activation in Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2022Article
- Nonplatelet thromboxane generation is associated with impaired cardiovascular performance and mortality in heart failure.American journal of physiology. Heart and circulatory physiology · 2022Article
- The thromboxane receptor antagonistFrontiers in cardiovascular medicine · 2022Article
- N-Terminal Pro-Brain Natriuretic Peptide and Right Ventricular Diameter Are Related to Aspirin Resistance in Coronary Artery Disease Patients.Medicina (Kaunas, Lithuania) · 2021Article
- NTP42, a novel antagonist of the thromboxane receptor, attenuates experimentally induced pulmonary arterial hypertension.BMC pulmonary medicine · 2020Article
- Antagonism of the Thromboxane-Prostanoid Receptor as a Potential Therapy for Cardiomyopathy of Muscular Dystrophy.Journal of the American Heart Association · 2019Article
- A current view of G protein-coupled receptor - mediated signaling in pulmonary hypertension: finding opportunities for therapeutic intervention.Vessel plus · 2018Article
- rhACE2 Therapy Modifies Bleomycin-Induced Pulmonary Hypertension via Rescue of Vascular Remodeling.Frontiers in physiology · 2018Article
- Pressure overload leads to an increased accumulation and activity of mast cells in the right ventricle.Physiological reports · 2017Article
- Steps forward in the treatment of pulmonary arterial hypertension: latest developments and clinical opportunities.Therapeutic advances in chronic disease · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Right ventricular (RV) failure is the primary cause of death in pulmonary arterial hypertension (PAH) and is a significant cause of morbidity and mortality in other forms of pulmonary hypertension. There are no approved therapies directed at preserving RV function. F-series and E-series isoprostanes are increased in heart failure and PAH, correlate to the severity of disease, and can signal through the thromboxane-prostanoid (TP) receptor, with effects from vasoconstriction to fibrosis. The goal of these studies was to determine whether blockade of the TP receptor with the antagonist CPI211 was beneficial therapeutically in PAH-induced RV dysfunction. Mice with RV dysfunction due to pressure overload by pulmonary artery banding (PAB) were given vehicle or CPI211. Two weeks after PAB, CPI211-treated mice were protected from fibrosis with pressure overload. Gene expression arrays and immunoblotting, quantitative histology and morphometry, and flow cytometric analysis were used to determine the mechanism of CPI211 protection. TP receptor inhibition caused a near normalization of fibrotic area, prevented cellular hypertrophy while allowing increased RV mass, increased expression of antifibrotic thrombospondin-4, and blocked induction of the profibrotic transforming growth factor β (TGF-β) pathway. A thromboxane synthase inhibitor or low-dose aspirin failed to replicate these results, which suggests that a ligand other than thromboxane mediates fibrosis through the TP receptor after pressure overload. This study suggests that TP receptor antagonism may improve RV adaptation in situations of pressure overload by decreasing fibrosis and TGF-β signaling.
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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.