Pulmonary arterial hypertension (PAH) is a devastating disease without effective drugs available for its treatment. An in-depth exploration of the pathogenesis of PAH, as well as inquiry into potential therapeutic targets, remains an urgent issue. Non-coding RNAs (ncRNAs) have arisen as key players in malignant tumors, cardiovascular diseases and more recently in PAH progression and development. Network pharmacology is a new discipline based on system biology, which can predict potential therapeutic targets in diseases regulated by multiple genes. In this review, we discuss the current knowledge of ncRNAs and network pharmacology regulated genes involved in PAH, as well as the search for potential drug targets for PAH.
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Simulation of clinical trials of oral treprostinil in pulmonary arterial hypertension using a virtual population.
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January 2025
United Therapeutics Corporation, Silver Spring, MD, USA.
Challenges in drug development for rare diseases such as pulmonary arterial hypertension can be addressed through the use of mathematical modeling. In this study, a quantitative systems pharmacology model of pulmonary arterial hypertension pathophysiology and pharmacology was used to predict changes in pulmonary vascular resistance and six-minute walk distance in the context of oral treprostinil clinical studies. We generated a virtual population that spanned the range of clinical observations and then calibrated virtual patient-specific weights to match clinical trials.
View Article and Find Full Text PDFPulmonary Arterial Hypertension Incidence in Scleroderma Patients Treated with Bosentan for Digital Ulcers: Evidence from the Italian SPRING Registry.
J Rheumatol
January 2025
Florenzo Iannone, Rheumatology Unit - Department of Precision and Regenerative Medicine of Jonian Area University of Bari, Bari, Italy.
Objective: Bosentan (BOS) is approved for treating pulmonary arterial hypertension (PAH) and preventing digital ulcers (DU) in systemic sclerosis (SSc). Our study aimed to evaluate whether BOS prescribed for DU could reduce the incidence of PAH in a large SSc cohort from the SPRING registry.
Methods: Patients with SSc from the SPRING registry, meeting ACR/EULAR 2013 classification criteria with data on PAH onset, DU status, BOS exposure, and at least a one-year follow-up between 2015 and 2020, and no known PAH at baseline were included.
Right Ventricular Function and Outcomes Stratified by the Effective Regurgitant Orifice Area in Secondary Tricuspid Regurgitation.
Can J Cardiol
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Department of Cardiology, Istituto Auxologico Italiano, IRCCS, Milan, Italy; Department of Medicine and Surgery, University of Milano- Bicocca, Milan, Italy.
Background: In patients with moderate and severe secondary tricuspid regurgitation (STR), the effective regurgitant orifice area (EROA), corrected using the proximal isovelocity surface area (PISA) method for tricuspid valve leaflet tethering and low TR jet velocities, has an unclear threshold for identifying high-risk patients. This study aimed to establish a risk-based EROA cutoff and assess the impact of right ventricular (RV) remodeling on outcomes in low-risk STR patients according to EROA.
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Safety and Efficacy of Selexipag for Pediatric Pulmonary Arterial Hypertension in Japanese Patients - An Open-Label Phase 2 Study.
Circ J
January 2025
Department of Echo-imaging Center, Aizawa Hospital.
Background: Selexipag, an oral prostacyclin (PGI) receptor agonist, is approved for adult patients with pulmonary arterial hypertension (PAH). This study evaluated the efficacy and safety of selexipag for Japanese pediatric patients with PAH.
Methods And Results: The study enrolled 6 patients who received selexipag twice daily at an individualized dose based on body weight; maintenance doses were determined for each patient by 12 weeks after starting administration.
1,8-Cineole reduces pulmonary vascular remodelling in pulmonary arterial hypertension by restoring intercellular communication and inhibiting angiogenesis.
Phytomedicine
December 2024
Univ Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Azinhaga de S. Comba, Coimbra 3000-548, Portugal; Univ Coimbra, Center for Innovative Biomedicine and Biotechnology (CIBB), Coimbra, Portugal; Clinical Academic Centre of Coimbra (CACC), Coimbra, Portugal.
Background: Pulmonary Arterial Hypertension (PAH) is characterized by pulmonary vascular remodelling, often associated with disruption of BMPR2/Smad1/5 and BMPR2/PPAR-γ signalling pathways that ultimately lead to right ventricle failure. Disruption of intercellular junctions and communication and a pro-angiogenic environment are also characteristic features of PAH. Although, current therapies improve pulmonary vascular tone, they fail to tackle other key pathological features that could prevent disease progression.
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