ArticleBritish journal of pharmacology2018
Efficacy of treprostinil in the SU5416-hypoxia model of severe pulmonary arterial hypertension: haemodynamic benefits are not associated with improvements in arterial remodelling.
Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Mapping disease-specific vascular cell populations responsible for obliterative arterial remodelling during the development of pulmonary arterial hypertension.Cardiovascular research · 2025Article
- Cardioprotective effects of extracellular vesicles from hypoxia-preconditioned mesenchymal stromal cells in experimental pulmonary arterial hypertension.Stem cell research & therapy · 2025Article
- Current Overview of the Biology and Pharmacology in Sugen/Hypoxia-Induced Pulmonary Hypertension in Rats.Journal of aerosol medicine and pulmonary drug delivery · 2024Review
- Hepatic ischemia-reperfusion syndrome and its effect on the cardiovascular system: The role of treprostinil, a synthetic prostacyclin analog.World journal of gastrointestinal surgery · 2023Review
- The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023Review
- Article
- Inhibition of JAK1,2 Prevents Fibrotic Remodeling of Pulmonary Vascular Bed and Improves Outcomes in the Rat Model of Chronic Thromboembolic Pulmonary Hypertension.International journal of molecular sciences · 2022Article
- Penetrance of Severe Pulmonary Arterial Hypertension in Response to Vascular Endothelial Growth Factor Receptor 2 Blockade in a Genetically Prone Rat Model Is Reduced by Female Sex.Journal of the American Heart Association · 2021Article
- Prostaglandin I2 signaling licenses Treg suppressive function and prevents pathogenic reprogramming.The Journal of clinical investigation · 2021Article
- Characterisation of cough evoked by inhaled treprostinil and treprostinil palmitil.ERJ open research · 2021Article
- MicroRNA‑15a‑5p induces pulmonary artery smooth muscle cell apoptosis in a pulmonary arterial hypertension model via the VEGF/p38/MMP‑2 signaling pathway.International journal of molecular medicine · 2020Article
- Morphological and Functional Characteristics of Animal Models of Myocardial Fibrosis Induced by Pressure Overload.International journal of hypertension · 2020Review
- The selective PGI2 receptor agonist selexipag ameliorates Sugen 5416/hypoxia-induced pulmonary arterial hypertension in rats.PloS one · 2020Article
- Effects of the FGF receptor-1 inhibitor, infigratinib, with or without sildenafil, in experimental pulmonary arterial hypertension.British journal of pharmacology · 2019Article
- Efficacy of treprostinil in the SU5416-hypoxia model of severe pulmonary arterial hypertension: haemodynamic benefits are not associated with improvements in arterial remodelling.British journal of pharmacology · 2018Article
- The Role of G Protein-Coupled Receptors in the Right Ventricle in Pulmonary Hypertension.Frontiers in cardiovascular medicine · 2018Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposePulmonary arterial hypertension (PAH) is a life-threatening disease that leads to progressive pulmonary hypertension, right heart failure and death. Parenteral prostaglandins (PGs), including treprostinil, a prostacyclin analogue, represent the most effective medical treatment for severe PAH. We investigated the effect of treprostinil on established severe PAH and underlying mechanisms using the rat SU5416 (SU, a VEGF receptor-2 inhibitor)-chronic hypoxia (Hx) model of PAH. EXPERIMENTAL APPROACH: Male Sprague Dawley rats were injected with SU (20 mg·kg KEY
resultsAt week 7, no difference in RVSP or RV hypertrophy was observed between vehicle and Trep-100; however, Trep-810 significantly reduced RVSP and RV hypertrophy. Trep-810 treatment significantly improved cardiac structure and function. Further, a short-term infusion of treprostinil in rats with established PAH at 4 weeks post-SU produced an acute, dose-dependent reduction in RVSP consistent with a vasodilator effect. However, chronic Trep-810 treatment did not alter media wall thickness, degree of vascular occlusion or total vessel count in the lungs. CONCLUSIONS AND IMPLICATIONS: Treprostinil exerts therapeutic benefits in PAH through decreased vascular resistance and improved cardiac structure and function; however, treprostinil treatment does not have direct impact vascular remodelling.
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