ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
NFAT is required for spontaneous pulmonary hypertension in superoxide dismutase 1 knockout mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Interferon receptor gene dosage differentially regulates hypoxia-induced platelet activation and pulmonary hypertension in down syndrome.Frontiers in immunology · 2026Article
- Inducible Ift88-deficient mice show features consistent with mild pulmonary hypertension.Physiological reports · 2026Article
- Omega-3 polyunsaturated fatty acids and pulmonary arterial hypertension: Insights and perspectives.European journal of clinical investigation · 2024Review
- 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
- Vasoconstrictor Mechanisms in Chronic Hypoxia-Induced Pulmonary Hypertension: Role of Oxidant Signaling.Antioxidants (Basel, Switzerland) · 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
- Alteration of Extracellular Superoxide Dismutase in Idiopathic Pulmonary Arterial Hypertension.Frontiers in medicine · 2020Article
- miR-1 induces endothelial dysfunction in rat pulmonary arteries.Journal of physiology and biochemistry · 2019Article
- Redox Biology of Peroxisome Proliferator-Activated Receptor-γ in Pulmonary Hypertension.Antioxidants & redox signaling · 2019Review
- Redox Regulation of Ion Channels and Receptors in Pulmonary Hypertension.Antioxidants & redox signaling · 2019Review
- Role of Gender in Regulation of Redox Homeostasis in Pulmonary Arterial Hypertension.Antioxidants (Basel, Switzerland) · 2019Review
- Mechanisms contributing to persistently activated cell phenotypes in pulmonary hypertension.The Journal of physiology · 2019Review
- Mitochondrial dysfunction and pulmonary hypertension: cause, effect, or both.American journal of physiology. Lung cellular and molecular physiology · 2018Review
- Inhibition of nuclear factor of activated T cells (NFAT) c3 activation attenuates acute lung injury and pulmonary edema in murine models of sepsis.Oncotarget · 2018Article
- Hypoxia induces pulmonary fibroblast proliferation through NFAT signaling.Scientific reports · 2018Article
- Reactive Oxygen and Nitrogen Species in the Development of Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2017Review
- Central role of T helper 17 cells in chronic hypoxia-induced pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- The role of nuclear factor of activated T cells in pulmonary arterial hypertension.Cell cycle (Georgetown, Tex.) · 2017Review
- Contribution of reactive oxygen species to the pathogenesis of pulmonary arterial hypertension.PloS one · 2017Article
- ASIC1-mediated calcium entry stimulates NFATc3 nuclear translocation via PICK1 coupling in pulmonary arterial smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Elevated reactive oxygen species are implicated in pulmonary hypertension (PH). Superoxide dismutase (SOD) limits superoxide bioavailability, and decreased SOD activity is associated with PH. A decrease in SOD activity is expected to increase superoxide and reduce hydrogen peroxide levels. Such an imbalance of superoxide/hydrogen peroxide has been implicated as a mediator of nuclear factor of activated T cells (NFAT) activation in epidermal cells. We have shown that NFATc3 is required for chronic hypoxia-induced PH. However, it is unknown whether NFATc3 is activated in the pulmonary circulation in a mouse model of decreased SOD1 activity and whether this leads to PH. Therefore, we hypothesized that an elevated pulmonary arterial superoxide/hydrogen peroxide ratio activates NFATc3, leading to PH. We found that SOD1 knockout (KO) mice have elevated pulmonary arterial wall superoxide and decreased hydrogen peroxide levels compared with wild-type (WT) littermates. Right ventricular systolic pressure (RVSP) was elevated in SOD1 KO and was associated with pulmonary arterial remodeling. Vasoreactivity to endothelin-1 was also greater in SOD1 KO vs. WT mice. NFAT activity and NFATc3 nuclear localization were increased in pulmonary arteries from SOD1 KO vs. WT mice. Administration of A-285222 (selective NFAT inhibitor) decreased RVSP, arterial wall thickness, vasoreactivity, and NFAT activity in SOD1 KO mice to WT levels. The SOD mimetic, tempol, also reduced NFAT activity, NFATc3 nuclear localization, and RVSP to WT levels. These findings suggest that an elevated superoxide/hydrogen peroxide ratio activates NFAT in pulmonary arteries, which induces vascular remodeling and increases vascular reactivity leading to PH.
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