ArticleCirculation research2026
Endothelial ADAR1 Deficit Induces the NOCT-IRF7 Axis in Pulmonary Hypertension.
Article in Circulation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Global knockout of melanoma differentiation-associated protein 5 protects mice from chronic hypoxia/SU5416-induced pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Adenosine-to-Inosine (A-to-I) RNA Editing by ADAR1 to Control RNA Sensing in Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Circadian control of immune homeostasis in cardiovascular health and disease.Frontiers in immunology · 2026Review
- Neonatal pulmonary vascular remodeling induced by increased blood flow is associated with an antiviral-like immune signature.Frontiers in immunology · 2026Article
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28 authors.
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Abstract
backgroundEarly apoptosis of pulmonary artery endothelial cells (PAECs) is a driver of vascular remodeling and pulmonary hypertension (PH), but its regulation is poorly defined. Adenosine deaminase acting on RNA 1 (ADAR1, gene name
methodsADAR1 or Nocturnin (NOCT) expression and A-to-I RNA editing levels were evaluated in human PAH lungs by immunofluorescent staining and single cell RNA sequencing, respectively. Mice carrying a human missense
resultsADAR1 expression was downregulated in the pulmonary vascular endothelium and in lung tissue of human and mouse PH. Global A-to-I RNA editing was decreased in lungs from PAH patients and hypoxic PH mice. In vitro, hypoxia, a PH trigger, downregulated ADAR1 in PAECs. Circadian gene
conclusionsHypoxia-induced ADAR1 deficiency upregulates
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