ArticlePloS one2014
Local and systemic RAGE axis changes in pulmonary hypertension: CTEPH and iPAH.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Integrative single-cell RNA-seq and ATAC-seq analysis reveals the key role of inflammatory cell activation in pulmonary arterial hypertension.Frontiers in immunology · 2026Article
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- Experimental animal models of pulmonary hypertension: Development and challenges.Animal models and experimental medicine · 2022Article
- EGR1 Is Implicated in Right Ventricular Cardiac Remodeling Associated with Pulmonary Hypertension.Biology · 2022Article
- The Roles of S100A4 and the EGF/EGFR Signaling Axis in Pulmonary Hypertension with Right Ventricular Hypertrophy.Biology · 2022Article
- Soluble Receptor for Advanced Glycation End Products (sRAGE) Is a Sensitive Biomarker in Human Pulmonary Arterial Hypertension.International journal of molecular sciences · 2021Article
- Intravenous Delivery of Lung-Targeted Nanofibers for Pulmonary Hypertension in Mice.Advanced healthcare materials · 2021Article
- Identifying early pulmonary arterial hypertension biomarkers in systemic sclerosis: machine learning on proteomics from the DETECT cohort.The European respiratory journal · 2021Article
- Balloon pulmonary angioplasty for chronic thromboembolic pulmonary hypertension: State of the art.World journal of clinical cases · 2020Review
- AGE-RAGE Stress in the Pathophysiology of Pulmonary Hypertension and its Treatment.The International journal of angiology : official publication of the International College of Angiology, Inc · 2019Article
- Crucial role of RAGE in inappropriate increase of smooth muscle cells from patients with pulmonary arterial hypertension.PloS one · 2018Article
- Activation of PPARγ by baicalin attenuates pulmonary hypertension in an infant rat model by suppressing HMGB1/RAGE signaling.FEBS open bio · 2017Article
- Subclinical Atherosclerosis in Patients with Prior Pulmonary Thromboembolism.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2017Article
- Circulating biomarkers in chronic thromboembolic pulmonary hypertension.Pulmonary circulationArticle
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe molecular determinants of chronic thromboembolic pulmonary hypertension (CTEPH) and idiopathic pulmonary arterial hypertension (iPAH) remain poorly understood. The receptor for advanced glycation endproducts (RAGE) and its ligands: HMGB1 and S100A9 are involved in inflammatory disorders. We sought to investigate the role of the RAGE axis in patients with CTEPH undergoing pulmonary endarterectomy (PEA), iPAH undergoing lung transplantation (LuTX). The high pulmonary vascular resistance in CTEPH/iPAH results in pressure overload of the right ventricle. We compared sRAGE measurements to that of patients with aortic valve stenosis (AVS) - pressure overload of the left ventricle.
methodsWe enrolled patients with CTEPH(26), iPAH(15), AVS(15) and volunteers(33). Immunohistochemistry with antibodies to RAGE and HMGB1 was performed on PEA specimens and lung tissues. We employed enzyme-linked immunosorbent assays to determine the concentrations of sRAGE, esRAGE, HMGB1 and S100A9 in serum of volunteers and patients with CTEPH, iPAH, AVS before and after PEA, LuTX and aortic valve replacement (AVR).
resultsIn endarterectomised tissues from patients with CTEPH RAGE and HMGB1 were identified in myofibroblasts (α-SMA+vimentin+CD34-), recanalizing vessel-like structures of distal myofibrotic tissues and endothelium of neointima. RAGE was differentially expressed in prototypical Heath Edwards lesions in iPAH. We found significantly increased serum concentrations of sRAGE, esRAGE and HMGB1 in CTEPH. In iPAH, sRAGE and esRAGE were significantly higher than in controls. Serum concentrations of sRAGE were significantly elevated in iPAH(p<0.001) and CTEPH(p = 0.001) compared to AVS. Serum sRAGE was significantly higher in iPAH compared to CTEPH(p = 0.042) and significantly reduced in AVS compared to controls(p = 0.001). There were no significant differences in sRAGE serum concentrations before and after surgical therapy for CTEPH, iPAH or AVS.
conclusionsOur data suggest a role for the RAGE pathway in the pathophysiology of CTEPH and iPAH. PEA improves the local control of disease but may not influence the systemic inflammatory mechanisms in CTEPH patients through the RAGE pathway.
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