ReviewInternational journal of molecular sciences2019
Molecular Research in Chronic Thromboembolic Pulmonary Hypertension.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Methylation in the TAC1 Gene Promoter Is Associated with the Transition from Acute Pulmonary Embolism to Chronic Thromboembolic Pulmonary Hypertension.International journal of molecular sciences · 2026Article
- Observational
- MicroRNA expression alteration in chronic thromboembolic pulmonary hypertension: A systematic review.Pulmonary circulation · 2024Article
- Chronic thromboembolic pulmonary hypertension: the diagnostic assessment.Frontiers in cardiovascular medicine · 2024Review
- Loss of Amphiregulin drives inflammation and endothelial apoptosis in pulmonary hypertension.Life science alliance · 2022Article
- Diagnostic value of miRNA expression and right ventricular echocardiographic functional parameters for chronic thromboembolic pulmonary hypertension with right ventricular dysfunction and injury.BMC pulmonary medicine · 2022Article
- LncRNA-GAS5/miR-382-3p axis inhibits pulmonary artery remodeling and promotes autophagy in chronic thromboembolic pulmonary hypertension.Genes & genomics · 2022Article
- MiR-34a-3p suppresses pulmonary vascular proliferation in acute pulmonary embolism rat by targeting DUSP1.Bioscience reports · 2022Article
- Single-cell RNA-sequencing and microarray analyses to explore the pathological mechanisms of chronic thromboembolic pulmonary hypertension.Frontiers in cardiovascular medicine · 2022Article
- Article
- Chronic Thromboembolic Pulmonary Hypertension - What Have We Learned From Large Animal Models.Frontiers in cardiovascular medicine · 2021Review
- Expression of miR-93-5p as a Potential Predictor of the Severity of Chronic Thromboembolic Pulmonary Hypertension.BioMed research international · 2021Article
- Myeloproliferative Diseases as Possible Risk Factor for Development of Chronic Thromboembolic Pulmonary Hypertension-A Genetic Study.International journal of molecular sciences · 2020Article
- miR‑106b‑5p modulates acute pulmonary embolism via NOR1 in pulmonary artery smooth muscle cells.International journal of molecular medicine · 2020Article
- The Biological Bases of Group 2 Pulmonary Hypertension.International journal of molecular sciences · 2019Review
- hsa-miR-106b-5p participates in the development of chronic thromboembolic pulmonary hypertension via targeting matrix metalloproteinase 2.Pulmonary circulationArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic Thromboembolic Pulmonary Hypertension (CTEPH) is a debilitating disease, for which the underlying pathophysiological mechanisms have yet to be fully elucidated. Occurrence of a pulmonary embolism (PE) is a major risk factor for the development of CTEPH, with non-resolution of the thrombus being considered the main cause of CTEPH. Polymorphisms in the α-chain of fibrinogen have been linked to resistance to fibrinolysis in CTEPH patients, and could be responsible for development and disease progression. However, it is likely that additional genetic predisposition, as well as genetic and molecular alterations occurring as a consequence of tissue remodeling in the pulmonary arteries following a persistent PE, also play an important role in CTEPH. This review summarises the current knowledge regarding genetic differences between CTEPH patients and controls (with or without pulmonary hypertension). Mutations in BMPR2, differential gene and microRNA expression, and the transcription factor FoxO1 have been suggested to be involved in the processes underlying the development of CTEPH. While these studies provide the first indications regarding important dysregulated pathways in CTEPH (e.g., TGF-β and PI3K signaling), additional in-depth investigations are required to fully understand the complex processes leading to 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.