ArticleAmerican journal of respiratory and critical care medicine2019
FHIT, a Novel Modifier Gene in Pulmonary Arterial Hypertension.
Article in American journal of respiratory and critical care medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 48 citations in OpenAlex.
- Metabolic Markers as Potential Risk Factors in Pulmonary Hypertension.Pulmonary circulation · 2026Article
- Lung Single-Cell Transcriptomics Reveal Diverging Pathobiology and Opportunities for Precision Targeting in Scleroderma-Associated Versus Idiopathic Pulmonary Arterial Hypertension.Circulation. Genomic and precision medicine · 2025Article
- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- Association of FHIT gene variant and salty food preference with the incidence of metabolic syndrome.Genes & nutrition · 2025Article
- 3D Imaging Reveals Complex Microvascular Remodeling in the Right Ventricle in Pulmonary Hypertension.Circulation research · 2024Article
- Review
- Review
- Article
- Whole-Genome Sequencing of 100 Genomes Identifies a Distinctive Genetic Susceptibility Profile of Qatari Patients with Hypertension.Journal of personalized medicine · 2022Article
- Construction of a diagnostic signature and immune landscape of pulmonary arterial hypertension.Frontiers in cardiovascular medicine · 2022Article
- Repurposing drug molecules for new pulmonary therapeutic interventions.Drug delivery and translational research · 2021Review
- iPSC-endothelial cell phenotypic drug screening and in silico analyses identify tyrphostin-AG1296 for pulmonary arterial hypertension.Science translational medicine · 2021Article
- Identification of Copy Number Variation Among Nonsyndromic Cleft Lip and or Without Cleft Palate With Hypodontia: A Genome-Wide Association Study.Frontiers in physiology · 2021Article
- Review
- Review
- Targeting BMPR2 Trafficking with Chaperones: An Important Step toward Precision Medicine in Pulmonary Arterial Hypertension.American journal of respiratory cell and molecular biology · 2020Article
- Update in Pulmonary Vascular Diseases and Right Ventricular Dysfunction 2019.American journal of respiratory and critical care medicine · 2020Article
- The hallmarks of severe pulmonary arterial hypertension: the cancer hypothesis-ten years later.American journal of physiology. Lung cellular and molecular physiology · 2020Review
- The role of genomics and genetics in pulmonary arterial hypertension.Global cardiology science & practice · 2020Review
- The fission yeast FHIT homolog affects checkpoint control of proliferation and is regulated by mitochondrial electron transport.Cell biology international · 2020Article
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Authors and funding
19 authors at 6 institutions in 2 countries.
Funding
Abstract
rationalePulmonary arterial hypertension (PAH) is characterized by progressive narrowing of pulmonary arteries, resulting in right heart failure and death. BMPR2 (bone morphogenetic protein receptor type 2) mutations account for most familial PAH forms whereas reduced BMPR2 is present in many idiopathic PAH forms, suggesting dysfunctional BMPR2 signaling to be a key feature of PAH. Modulating BMPR2 signaling is therapeutically promising, yet how BMPR2 is downregulated in PAH is unclear.
objectivesWe intended to identify and pharmaceutically target BMPR2 modifier genes to improve PAH.
methodsWe combined siRNA high-throughput screening of >20,000 genes with a multicohort analysis of publicly available PAH RNA expression data to identify clinically relevant BMPR2 modifiers. After confirming gene dysregulation in tissue from patients with PAH, we determined the functional roles of BMPR2 modifiers in vitro and tested the repurposed drug enzastaurin for its propensity to improve experimental pulmonary hypertension (PH). MEASUREMENTS AND MAIN
resultsWe discovered FHIT (fragile histidine triad) as a novel BMPR2 modifier. BMPR2 and FHIT expression were reduced in patients with PAH. FHIT reductions were associated with endothelial and smooth muscle cell dysfunction, rescued by enzastaurin through a dual mechanism: upregulation of FHIT as well as miR17-5 repression. Fhit
conclusionsThis study highlights the importance of the novel BMPR2 modifier FHIT in PH and the clinical value of the repurposed drug enzastaurin as a potential novel therapeutic strategy to improve PAH.
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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.