ArticleScientific reports2024
Exploring the Endothelin-1 pathway in chronic thromboembolic pulmonary hypertension microvasculopathy.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Serum Endothelin-1 in Suspected Acute Pulmonary Embolism: A Prospective Study.Journal of cardiovascular development and disease · 2026Article
- Minimally Invasive Porcine Model for Chronic Thromboembolic Pulmonary Hypertension.Pulmonary circulation · 2026Article
- Chronic Thromboembolic Pulmonary Hypertension as an Inflammation-Angiogenesis Disorder: From Thrombus Persistence to Dual Pulmonary Vasculopathy.Reviews in cardiovascular medicine · 2026Review
- The MCP-1/CCR2-CD16⁺ monocyte axis drives thrombus fibrosis in Chronic Thromboembolic Pulmonary Hypertension.Journal of translational medicine · 2026Article
- Flavonoids: Potential New Drug Candidates for Attenuating Vascular Remodeling in Pulmonary Hypertension.International journal of molecular sciences · 2025Review
- The Involvement of Endothelin-1 in Sepsis and Organ Dysfunction-A Novel Biomarker in Patient Assessment.Biomedicines · 2025Review
- Effects of sildenafil and metformin on endothelin-1 in the progression of pulmonary hypertension.Open veterinary journal · 2025Article
- A swine model of severe chronic thromboembolic pulmonary hypertension induced by repeated pulmonary artery long suture injection.Frontiers in cardiovascular medicine · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeted vasopeptide therapies have significantly advanced the management of pulmonary arterial hypertension (PAH). However, due to insufficient preclinical evidence regarding the involvement of the endothelin-1 (ET-1) pathway in chronic thromboembolic pulmonary hypertension (CTEPH) pathophysiology, the potential of ET-1 receptor antagonism in treating CTEPH remains uncertain. In this study, we investigated the role of the ET-1 pathway in CTEPH microvasculopathy using a multifaceted approach. Plasma ET-1 levels were measured in a cohort of 59 CTEPH patients and 41 healthy controls. Additionally, we evaluated the expression of key ET-1 pathway members in pulmonary explants from CTEPH, idiopathic PAH, and control patients. We used an in vitro system to test the hypothesis that the turbulent flow, observed near the vascular obstructions pathognomonic of CTEPH, enhances ET-1 expression. Our findings were further validated in vivo using a CTEPH piglet model that contains distinct regions representing pre- and post-thrombus lung territories. We found a twofold increase in circulating ET-1 levels in CTEPH patients compared to healthy subjects. Pulmonary explants from CTEPH patients exhibited pronounced overexpression of ET-1, endothelin receptor A (ET
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