ArticleCells2021
The Inflammatory Profile of CTEPH-Derived Endothelial Cells Is a Possible Driver of Disease Progression.
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- The Impact of Balloon Pulmonary Angioplasty (BPA) on Changes in the Liver Fibrosis Index (FIB-4 Index) in Patients with Chronic Thromboembolic Pulmonary Hypertension (CTEPH).Journal of clinical medicine · 2026Article
- The predictive value of the systemic immune-inflammation index in chronic thromboembolic pulmonary hypertension.Medicine · 2026Article
- Research advances in chronic thromboembolic pulmonary hypertension: from pathological mechanisms to multidisciplinary management.Frontiers in cardiovascular medicine · 2026Review
- Overexpression of PRDX2 alleviates chronic thromboembolic pulmonary hypertension by modulating inflammation and mitophagy.Scientific reports · 2025Article
- Circulating Pin1 Levels in Patients With Chronic Thromboembolic Pulmonary Hypertension: A Case-Control Study.Pulmonary circulation · 2025Article
- The Role of the Pulmonary Vascular Microenvironment in Chronic Thromboembolic Pulmonary Hypertension.Pulmonary circulation · 2025Review
- New insights into pulmonary arterial hypertension: interaction between PANoptosis and perivascular inflammatory responses.Apoptosis : an international journal on programmed cell death · 2025Review
- Natural terpenoids with therapeutic potential against pulmonary arterial hypertension.Frontiers in pharmacology · 2025Review
- Association of Systemic Inflammatory Response Index with Disease Severity and Adverse Outcome in Chronic Thromboembolic Pulmonary Hypertension.Journal of inflammation research · 2025Article
- Pulmonary Hypertension: Pharmacological and Non-Pharmacological Therapies.Life (Basel, Switzerland) · 2024Review
- Controlling Nutritional Status Score Predicts 1-Year Outcomes in Chronic Thromboembolic Pulmonary Hypertension.Circulation reports · 2024Article
- CC chemokines Modulate Immune responses in Pulmonary Hypertension.Journal of advanced research · 2024Review
- Pulmonary Hypertension and the Gut Microbiome.Biomedicines · 2024Review
- Analysis of genes characterizing chronic thrombosis and associated pathways in chronic thromboembolic pulmonary hypertension.PloS one · 2024Article
- Endothelial Overexpression of TGF-β-Induced Protein Impairs Venous Thrombus Resolution: Possible Role in CTEPH.JACC. Basic to translational science · 2024Article
- ERS International Congress 2023: highlights from the Pulmonary Vascular Diseases Assembly.ERJ open research · 2024Article
- The significance of CD16+ monocytes in the occurrence and development of chronic thromboembolic pulmonary hypertension: insights from single-cell RNA sequencing.Frontiers in immunology · 2024Article
- Chronic Thromboembolic Pulmonary Hypertension: A Review of the Multifaceted Pathobiology.Biomedicines · 2023Review
- Mechanism of piR-1245/PIWI-like protein-2 regulating Janus kinase-2/signal transducer and activator of transcription-3/vascular endothelial growth factor signaling pathway in retinal neovascularization.Neural regeneration research · 2023Article
- Peri-Operative Changes of Inflammatory Markers and Their Implications in Pulmonary Endarterectomy.Reviews in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Chronic thromboembolic pulmonary hypertension (CTEPH) is a form of pulmonary hypertension characterized by the presence of fibrotic intraluminal thrombi and causing obliteration of the pulmonary arteries. Although both endothelial cell (EC) dysfunction and inflammation are linked to CTEPH pathogenesis, regulation of the basal inflammatory response of ECs in CTEPH is not fully understood. Therefore, in the present study, we investigated the role of the nuclear factor (NF)-κB pro-inflammatory signaling pathway in ECs in CTEPH under basal conditions. Basal mRNA levels of interleukin (IL)-8, IL-1β, monocyte chemoattractant protein-1 (MCP-1), C-C motif chemokine ligand 5 (CCL5), and vascular cell adhesion molecule-1 (VCAM-1) were upregulated in CTEPH-ECs compared to the control cells. To assess the involvement of NF-κB signaling in basal inflammatory activation, CTEPH-ECs were incubated with the NF-κB inhibitor Bay 11-7085. The increase in pro-inflammatory cytokines was abolished when cells were incubated with the NF-κB inhibitor. To determine if NF-κB was indeed activated, we stained pulmonary endarterectomy (PEA) specimens from CTEPH patients and ECs isolated from PEA specimens for phospho-NF-κB-P65 and found that especially the vessels within the thrombus and CTEPH-ECs are positive for phospho-NF-κB-P65. In summary, we show that CTEPH-ECs have a pro-inflammatory status under basal conditions, and blocking NF-κB signaling reduces the production of inflammatory factors in CTEPH-ECs. Therefore, our results show that the increased basal pro-inflammatory status of CTEPH-ECs is, at least partially, regulated through activation of NF-κB signaling and potentially contributes to the pathophysiology and progression of 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 OpenQuestion graph.