ArticleScientific reports2021
Derivation and characterisation of endothelial cells from patients with chronic thromboembolic pulmonary hypertension.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Chronic Thromboembolic Pulmonary Hypertension as an Inflammation-Angiogenesis Disorder: From Thrombus Persistence to Dual Pulmonary Vasculopathy.Reviews in cardiovascular medicine · 2026Review
- Understanding the Impact of Hypoxia on Pulmonary Artery Endothelial Cells in Chronic Thromboembolic Pulmonary Hypertension Patients.International journal of molecular sciences · 2026Article
- Increased lung [The European respiratory journal · 2025Article
- Role of Extracellular Vesicles in Chronic Post-Embolic Pulmonary Hypertension: Data from an Experimental Animal Model and Patients.Biomedicines · 2025Article
- Physiological shear stress suppresses apoptosis in human pulmonary microvascular endothelial cells.Physiological reports · 2025Article
- Hypoxia Combined With Interleukin-17 Regulates Hypoxia-Inducible Factor-1α/Endothelial Nitric Oxide Synthase Expression in Pulmonary Artery Endothelial Cells.Journal of cellular and molecular medicine · 2025Article
- Vitamin D receptor and its antiproliferative effect in human pulmonary arterial hypertension.Scientific reports · 2024Article
- The Relevance of the Endothelium in Cardiopulmonary Disorders.International journal of molecular sciences · 2024Review
- Oxidative stress in acute pulmonary embolism: emerging roles and therapeutic implications.Thrombosis journal · 2024Review
- Mitochondria-derived Vesicle Packaging as a Novel Therapeutic Mechanism in Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2024Article
- Endothelial Overexpression of TGF-β-Induced Protein Impairs Venous Thrombus Resolution: Possible Role in CTEPH.JACC. Basic to translational science · 2024Article
- Analysis of genes characterizing chronic thrombosis and associated pathways in chronic thromboembolic pulmonary hypertension.PloS one · 2024Article
- Hyperactive mTORC1 in lung mesenchyme induces endothelial cell dysfunction and pulmonary vascular remodeling.The Journal of clinical investigation · 2023Article
- Oxidative Stress and Antioxidant Therapy in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2023Review
- Sympathetic Denervation and Pharmacological Stimulation of Parasympathetic Nervous System Prevent Pulmonary Vascular Bed Remodeling in Rat Model of Chronic Thromboembolic Pulmonary Hypertension.Journal of cardiovascular development and disease · 2023Article
- Metabolic profile in endothelial cells of chronic thromboembolic pulmonary hypertension and pulmonary arterial hypertension.Scientific reports · 2022Article
- Current Understanding of the Pivotal Role of Mitochondrial Dynamics in Cardiovascular Diseases and Senescence.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
Abstract
Pulmonary endarterectomy (PEA) resected material offers a unique opportunity to develop an in vitro endothelial cell model of chronic thromboembolic pulmonary hypertension (CTEPH). We aimed to comprehensively analyze the endothelial function, molecular signature, and mitochondrial profile of CTEPH-derived endothelial cells to better understand the pathophysiological mechanisms of endothelial dysfunction behind CTEPH, and to identify potential novel targets for the prevention and treatment of the disease. Isolated cells from specimens obtained at PEA (CTEPH-EC), were characterized based on morphology, phenotype, and functional analyses (in vitro and in vivo tubule formation, proliferation, apoptosis, and migration). Mitochondrial content, morphology, and dynamics, as well as high-resolution respirometry and oxidative stress, were also studied. CTEPH-EC displayed a hyperproliferative phenotype with an increase expression of adhesion molecules and a decreased apoptosis, eNOS activity, migration capacity and reduced angiogenic capacity in vitro and in vivo compared to healthy endothelial cells. CTEPH-EC presented altered mitochondrial dynamics, increased mitochondrial respiration and an unbalanced production of reactive oxygen species and antioxidants. Our study is the foremost comprehensive investigation of CTEPH-EC. Modulation of redox, mitochondrial homeostasis and adhesion molecule overexpression arise as novel targets and biomarkers in CTEPH.
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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 Socratic graph.