ArticleNature communications2019
The EYA3 tyrosine phosphatase activity promotes pulmonary vascular remodeling in pulmonary arterial hypertension.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
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- Single-nucleotide polymorphisms in dizygotic twin ovine fetuses are associated with discordant responses to antenatal steroid therapy.BMC medicine · 2025Article
- 'Cell knife' for cancer: the clinician's perspective.Frontiers in immunology · 2025Review
- Exploring the pathogenesis of pulmonary vascular disease.Frontiers in medicine · 2024Review
- Reduced FOXF1 links unrepaired DNA damage to pulmonary arterial hypertension.Nature communications · 2023Article
- Article
- Budesonide/glycopyrronium/formoterol fumarate triple therapy prevents pulmonary hypertension in a COPD mouse model via NFκB inactivation.Respiratory research · 2022Article
- Research Progress on Pulmonary Arterial Hypertension and the Role of the Angiotensin Converting Enzyme 2-Angiotensin-(1-7)-Mas Axis in Pulmonary Arterial Hypertension.Cardiovascular drugs and therapy · 2022Review
- Role and Diagnostic Performance of Host Epigenome in Respiratory Morbidity after RSV Infection: The EPIRESVi Study.Frontiers in immunology · 2022Observational
- Mechanism of Hypoxia-Mediated Smooth Muscle Cell Proliferation Leading to Vascular Remodeling.BioMed research international · 2022Review
- Expression of the microRNA-30 family in pulmonary arterial hypertension and the role of microRNA-30d-5p in the regulation of pulmonary arterial smooth muscle cell toxicity and apoptosis.Experimental and therapeutic medicine · 2022Article
- Cardiovascular risk associated with allopurinol vs. benzbromarone in patients with gout.European heart journal · 2021Article
- Nanoparticle Delivery of STAT3 Alleviates Pulmonary Hypertension in a Mouse Model of Alveolar Capillary Dysplasia.Circulation · 2021Article
- The Eyes Absent proteins in development and in developmental disorders.Biochemical Society transactions · 2021Review
- Targeting EYA3 in Ewing Sarcoma Retards Tumor Growth and Angiogenesis.Molecular cancer therapeutics · 2021Article
- The Eyes Absent Proteins: Unusual HAD Family Tyrosine Phosphatases.International journal of molecular sciences · 2021Review
- Inhibiting miR‑1 attenuates pulmonary arterial hypertension in rats.Molecular medicine reports · 2021Article
- Up-regulation of circRNA_0068481 promotes right ventricular hypertrophy in PAH patients via regulating miR-646/miR-570/miR-885.Journal of cellular and molecular medicine · 2021Article
- Endothelial Dec1-PPARγ Axis Impairs Proliferation and Apoptosis Homeostasis Under Hypoxia in Pulmonary Arterial Hypertension.Frontiers in cell and developmental biology · 2021Article
- CircGNG4 Promotes the Progression of Prostate Cancer by Sponging miR-223 to Enhance EYA3/c-myc Expression.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
In pulmonary hypertension vascular remodeling leads to narrowing of distal pulmonary arterioles and increased pulmonary vascular resistance. Vascular remodeling is promoted by the survival and proliferation of pulmonary arterial vascular cells in a DNA-damaging, hostile microenvironment. Here we report that levels of Eyes Absent 3 (EYA3) are elevated in pulmonary arterial smooth muscle cells from patients with pulmonary arterial hypertension and that EYA3 tyrosine phosphatase activity promotes the survival of these cells under DNA-damaging conditions. Transgenic mice harboring an inactivating mutation in the EYA3 tyrosine phosphatase domain are significantly protected from vascular remodeling. Pharmacological inhibition of the EYA3 tyrosine phosphatase activity substantially reverses vascular remodeling in a rat model of angio-obliterative pulmonary hypertension. Together these observations establish EYA3 as a disease-modifying target whose function in the pathophysiology of pulmonary arterial hypertension can be targeted by available inhibitors.
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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.