ArticleInternational journal of molecular medicine2014
Comparison of gene expression profiles and related pathways in chronic thromboembolic pulmonary hypertension.
Article in International journal of molecular medicine, 2014. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Observational
- From Pulmonary Embolism to Chronic Thromboembolic Pulmonary Hypertension: A Pathophysiological Approach.Reviews in cardiovascular medicine · 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 RNA-sequencing and microarray analyses to explore the pathological mechanisms of chronic thromboembolic pulmonary hypertension.Frontiers in cardiovascular medicine · 2022Article
- Revisiting a Distinct Entity in Pulmonary Vascular Disease: Chronic Thromboembolic Pulmonary Hypertension (CTEPH).Medicina (Kaunas, Lithuania) · 2021Review
- Effect of EZH2 on pulmonary artery smooth muscle cell migration in pulmonary hypertension.Molecular medicine reports · 2021Article
- Myeloproliferative Diseases as Possible Risk Factor for Development of Chronic Thromboembolic Pulmonary Hypertension-A Genetic Study.International journal of molecular sciences · 2020Article
- Article
- Analysis of lncRNA-miRNA-mRNA Interactions in Hyper-proliferative Human Pulmonary Arterial Smooth Muscle Cells.Scientific reports · 2019Article
- Molecular Research in Chronic Thromboembolic Pulmonary Hypertension.International journal of molecular sciences · 2019Review
- Chronic thromboembolic pulmonary hypertension.The European respiratory journal · 2019Review
- A Review of Transcriptome Analysis in Pulmonary Vascular Diseases.Methods in molecular biology (Clifton, N.J.) · 2018Article
- The pathophysiology of chronic thromboembolic pulmonary hypertension.European respiratory review : an official journal of the European Respiratory Society · 2017Review
- Identification of downstream target genes regulated by the nitric oxide-soluble guanylate cyclase-cyclic guanosine monophosphate signal pathway in pulmonary hypertension.The Journal of international medical research · 2016Article
- Aberrant expression of long noncoding RNAs in chronic thromboembolic pulmonary hypertension.Molecular medicine reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the main causes of severe pulmonary hypertension. However, despite treatment (pulmonary endarterectomy), in approximately 15-20% of patients, pulmonary vascular resistance and pulmonary arterial pressure continue to increase. To date, little is known about the changes that occur in gene expression in CTEPH. The identification of genes associated with CTEPH may provide insight into the pathogenesis of CTEPH and may aid in diagnosis and treatment. In this study, we analyzed the gene expresion profiles of pulmonary artery endothelial cells from 5 patients with CTEPH and 5 healthy controls using oligonucleotide microarrays. Bioinformatics analyses using the Gene Ontology (GO) and KEGG databases were carried out to identify the genes and pathways specifically associated with CTEPH. Signal transduction networks were established to identify the core genes regulating the progression of CTEPH. A number of genes were found to be differentially expressed in the pulmonary artery endothelial cells from patients with CTEPH. In total, 412 GO terms and 113 pathways were found to be associated with our list of genes. All differential gene interactions in the Signal-Net network were analyzed. JAK3, GNA15, MAPK13, ARRB2 and F2R were the most significantly altered. Bioinformatics analysis may help gather and analyze large amounts of data in microarrays by means of rigorous experimental planning, scientific statistical analysis and the collection of complete data. In this study, a novel differential gene expression pattern was constructed. However, further studies are required to identify novel targets for the diagnosis and treatment of CTEPH.
Indexed as
Identifiers
What OpenQuestion holds
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.