ArticlePloS one2012
Angiostatic factors in the pulmonary endarterectomy material from chronic thromboembolic pulmonary hypertension patients cause endothelial dysfunction.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 64 citations in OpenAlex.
- A single-cell census of pulmonary endarterectomies tissue across different anatomical regions in chronic thromboembolic pulmonary hypertension.Clinical and translational medicine · 2026Article
- Interferon receptor gene dosage differentially regulates hypoxia-induced platelet activation and pulmonary hypertension in down syndrome.Frontiers in immunology · 2026Article
- SOX17-silenced HPAECs upregulate NF-κB-induced CXCL10 and CXCL11: implications for lymphocyte chemotaxis in SOX17-PAH.Scientific reports · 2025Article
- Distinct endothelial cells in chronic thromboembolic pulmonary hypertension.NPJ cardiovascular health · 2025Article
- From Pulmonary Embolism to Chronic Thromboembolic Pulmonary Hypertension: A Pathophysiological Approach.Reviews in cardiovascular medicine · 2024Review
- Collagen 18A1/Endostatin Expression in the Progression of Right Ventricular Remodeling and Dysfunction in Pulmonary Arterial Hypertension.American journal of respiratory cell and molecular biology · 2024Article
- Role of platelet factor 4 in arteriovenous fistula maturation failure: What do we know so far?The journal of vascular access · 2024Review
- Endothelial Overexpression of TGF-β-Induced Protein Impairs Venous Thrombus Resolution: Possible Role in CTEPH.JACC. Basic to translational science · 2024Article
- Chronic Thromboembolic Pulmonary Hypertension: A Review of the Multifaceted Pathobiology.Biomedicines · 2023Review
- Article
- Single-Cell Analysis Reveals Distinct Immune and Smooth Muscle Cell Populations that Contribute to Chronic Thromboembolic Pulmonary Hypertension.American journal of respiratory and critical care medicine · 2023Article
- Article
- Pathophysiology and Treatment of Chronic Thromboembolic Pulmonary Hypertension.International journal of molecular sciences · 2023Review
- CXCL10 May Be Responsible for Susceptibility to Pulmonary Embolism in COVID-19 Patients.Journal of inflammation research · 2023Article
- CXCL10 levels in diagnosis and improved hemodynamics in patients with chronic thromboembolic pulmonary hypertension undergoing balloon pulmonary angioplasty.Pulmonary circulation · 2022Article
- From acute SARS-CoV-2 infection to pulmonary hypertension.Frontiers in physiology · 2022Review
- Modulation of soluble guanylate cyclase ameliorates pulmonary hypertension in a rat model of chronic thromboembolic pulmonary hypertension by stimulating angiogenesis.Physiological reports · 2022Article
- Chronic Thromboembolic Pulmonary Hypertension: the Bench.Current cardiology reports · 2021Review
- KCNK3 Mutation Causes Altered Immune Function in Pulmonary Arterial Hypertension Patients and Mouse Models.International journal of molecular sciences · 2021Article
- Endothelial Dysfunction in Pulmonary Hypertension: Cause or Consequence?Biomedicines · 2021Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare disease with persistent thrombotic occlusion or stenosis of the large pulmonary arteries resulting in pulmonary hypertension. Surgical removal of the neointimal layer of these vessels together with the non-resolved thrombus consisting of organized collagen-rich fibrotic areas with partly recanalized regions is the treatment of choice (pulmonary endarterectomy, PEA). The present study investigates endothelial cells isolated from such material as well as factors present in the surgical PEA material, which may contribute to impairment of recanalization and thrombus non-resolution. We observed muscularized vessels and non-muscularized vessels in the PEA material. The isolated endothelial cells from the PEA material showed significantly different calcium homeostasis as compared to pulmonary artery endothelial cells (hPAECs) from normal controls. In the supernatant (ELISA) as well as on the tissue level (histochemical staining) of the PEA material, platelet factor 4 (PF4), collagen type I and interferon-gamma-inducible 10 kD protein (IP-10) were detected. CXCR3, the receptor for PF4 and IP-10, was particularly elevated in the distal parts of the PEA material as compared to human control lung (RT-PCR). PF4, collagen type I and IP-10 caused significant changes in calcium homeostasis and affected the cell proliferation, migration and vessel formation in hPAECs. The presence of angiostatic factors like PF4, collagen type I and IP-10, as recovered from the surgical PEA material from CTEPH patients, may lead to changes in calcium homeostasis and endothelial dysfunction.
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