ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
NFATc3 is required for chronic hypoxia-induced pulmonary hypertension in adult and neonatal mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed.
- Understanding physiological adaptations of pregnancy to the chronic hypoxia of high altitude to inform obstetrical and neonatal care.Physiological reviews · 2026Review
- Identifying causal genetic variants for high-altitude adaptation through blood eQTL analysis in plateau populations.Communications biology · 2026Article
- Inducible Ift88-deficient mice show features consistent with mild pulmonary hypertension.Physiological reports · 2026Article
- Echocardiographic Assessment of Pulmonary Hemodynamics and Right Ventricular Performance in Neonatal Murine Hypoxia.Journal of cardiovascular development and disease · 2025Article
- A maternal hypoxia mouse model to study the effect of late gestational hypoxia on offspring lung outcomes.Frontiers in physiology · 2025Article
- Transcription factors and potential therapeutic targets for pulmonary hypertension.Frontiers in cell and developmental biology · 2023Review
- Chronic hypoxia disrupts T regulatory cell phenotype contributing to the emergence of exTreg-TFrontiers in physiology · 2023Article
- Genome ofInternational journal of molecular sciences · 2022Article
- Smooth muscle Acid-sensing ion channel 1a as a therapeutic target to reverse hypoxic pulmonary hypertension.Frontiers in molecular biosciences · 2022Article
- The Amniotic Fluid Cell-Free Transcriptome Provides Novel Information about Fetal Development and Placental Cellular Dynamics.International journal of molecular sciences · 2021Review
- MicroRNA‑153 attenuates hypoxia‑induced excessive proliferation and migration of pulmonary arterial smooth muscle cells by targeting ROCK1 and NFATc3.Molecular medicine reports · 2021Article
- Hypoxia-induced inhibition of mTORC1 activity in the developing lung: a possible mechanism for the developmental programming of pulmonary hypertension.American journal of physiology. Heart and circulatory physiology · 2021Article
- An Overview of miRNAs Involved in PASMC Phenotypic Switching in Pulmonary Hypertension.BioMed research international · 2021Review
- Oxidative Stress, Kinase Activation, and Inflammatory Pathways Involved in Effects on Smooth Muscle Cells During Pulmonary Artery Hypertension Under Hypobaric Hypoxia Exposure.Frontiers in physiology · 2021Review
- NFATc3 regulation of collagen V expression contributes to cellular immunity to collagen type V and hypoxic pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Cellular Pathways Promoting Pulmonary Vascular Remodeling by Hypoxia.Physiology (Bethesda, Md.) · 2020Review
- PKCβ and reactive oxygen species mediate enhanced pulmonary vasoconstrictor reactivity following chronic hypoxia in neonatal rats.American journal of physiology. Heart and circulatory physiology · 2020Article
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- Enhanced NO-dependent pulmonary vasodilation limits increased vasoconstrictor sensitivity in neonatal chronic hypoxia.American journal of physiology. Heart and circulatory physiology · 2017Article
- Soluble Epoxide Hydrolase Inhibition Protected against Angiotensin II-induced Adventitial Remodeling.Scientific reports · 2017Article
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9 authors.
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Abstract
Pulmonary hypertension occurs with prolonged exposure to chronic hypoxia in both adults and neonates. The Ca(2+)-dependent transcription factor, nuclear factor of activated T cells isoform c3 (NFATc3), has been implicated in chronic hypoxia-induced pulmonary arterial remodeling in adult mice. Therefore, we hypothesized that NFATc3 is required for chronic hypoxia-induced pulmonary hypertension in adult and neonatal mice. The aim of this study was to determine whether 1) NFATc3 mediates chronic hypoxia-induced increases in right ventricular systolic pressure in adult mice; 2) NFATc3 is activated in neonatal mice exposed to chronic hypoxia; and 3) NFATc3 is involved in chronic hypoxia-induced right ventricular hypertrophy and pulmonary vascular remodeling in neonatal mice. Adult mice were exposed to hypobaric hypoxia for 2, 7, and 21 days. Neonatal mouse pups were exposed for 7 days to hypobaric chronic hypoxia within 2 days after delivery. Hypoxia-induced increases in right ventricular systolic pressure were absent in NFATc3 knockout adult mice. In neonatal mice, chronic hypoxia caused NFAT activation in whole lung and nuclear accumulation of NFATc3 in both pulmonary vascular smooth muscle and endothelial cells. In addition, heterozygous NFATc3 neonates showed less right ventricular hypertrophy and pulmonary artery wall thickness in response to chronic hypoxia than did wild-type neonates. Our results suggest that NFATc3 mediates pulmonary hypertension and vascular remodeling in both adult and neonatal mice.
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