ArticleAmerican journal of physiology. Heart and circulatory physiology2010
NFATc3 contributes to intermittent hypoxia-induced arterial remodeling in mice.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Pulmonary Vascular Responses to Chronic Intermittent Hypoxia in a Guinea Pig Model of Obstructive Sleep Apnea.International journal of molecular sciences · 2024Article
- Simulated sleep apnea alters hydrogen sulfide regulation of blood flow and pressure.American journal of physiology. Heart and circulatory physiology · 2021Article
- Obstructive sleep apnoea and cardiovascular disease: a literature review.Archives of medical science : AMS · 2021Article
- Salidroside Ameliorated Intermittent Hypoxia-Aggravated Endothelial Barrier Disruption and AtherosclerosisFrontiers in pharmacology · 2021Article
- A dual blocker of endothelin A/B receptors mitigates hypertension but not renal dysfunction in a rat model of chronic kidney disease and sleep apnea.American journal of physiology. Renal physiology · 2019Article
- The role of the Nox4-derived ROS-mediated RhoA/Rho kinase pathway in rat hypertension induced by chronic intermittent hypoxia.Sleep & breathing = Schlaf & Atmung · 2017Article
- Chronic hypoxia alters fetal cerebrovascular responses to endothelin-1.American journal of physiology. Cell physiology · 2017Article
- NFAT regulation of cystathionine γ-lyase expression in endothelial cells is impaired in rats exposed to intermittent hypoxia.American journal of physiology. Heart and circulatory physiology · 2017Article
- Targeting the ROS-HIF-1-endothelin axis as a therapeutic approach for the treatment of obstructive sleep apnea-related cardiovascular complications.Pharmacology & therapeutics · 2016Review
- NFAT4-dependent miR-324-5p regulates mitochondrial morphology and cardiomyocyte cell death by targeting Mtfr1.Cell death & disease · 2015Article
- Article
- Amniotic fluid RNA gene expression profiling provides insights into the phenotype of Turner syndrome.Human genetics · 2014Article
- AKAP150 contributes to enhanced vascular tone by facilitating large-conductance Ca2+-activated K+ channel remodeling in hyperglycemia and diabetes mellitus.Circulation research · 2014Article
- Intermittent hypoxia-induced increases in reactive oxygen species activate NFATc3 increasing endothelin-1 vasoconstrictor reactivity.Vascular pharmacology · 2014Article
- Polymorphisms in nitric oxide synthase and endothelin genes among children with obstructive sleep apnea.BMC medical genomics · 2013Article
- Vasotrophic regulation of age-dependent hypoxic cerebrovascular remodeling.Current vascular pharmacology · 2013Review
- A less stressful alternative to oral gavage for pharmacological and toxicological studies in mice.Toxicology and applied pharmacology · 2012Article
- Endothelin-1 contributes to increased NFATc3 activation by chronic hypoxia in pulmonary arteries.American journal of physiology. Cell physiology · 2011Article
- Reactive oxygen species and the brain in sleep apnea.Respiratory physiology & neurobiology · 2010Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Sleep apnea (SA) is defined as intermittent respiratory arrest during sleep and affects up to 20% of the adult population. SA is also associated with an increased incidence of hypertension and peripheral vascular disease. Exposing rodents to intermittent hypoxia during sleep mimics the cyclical hypoxia/normoxia of SA. We have previously shown that in mice and rats intermittent hypoxia induces ET-1 upregulation and systemic hypertension. Furthermore, intermittent hypoxia (IH) in mice increases nuclear factor of activated T cells isoform 3 (NFATc3) transcriptional activity in aorta and mesenteric arteries, whereas the calcineurin/NFAT inhibitor cyclosporin A prevents IH-induced hypertension. More importantly, NFATc3 knockout (KO) mice do not develop IH-induced hypertension. The goals of this study were to determine the role of NFATc3 in IH-induced arterial remodeling and whether IH-induced NFATc3 activation is mediated by ET-1. Oral administration of both a dual (bosentan) and a selective endothelin receptor type A antagonist (PD155080) during 2 days of IH exposure attenuated NFAT activation in aorta and mesenteric arteries. Rho kinase inhibition with fasudil also prevented IH-induced NFAT activation. Mesenteric artery cross-sectional wall thickness was increased by IH in wild-type (WT) and vehicle-treated mice but not in bosentan-treated and NFATc3 KO mice. The arterial remodeling in mesenteric arteries after IH was characterized by increased expression of the hypertrophic NFATc3 target smooth muscle-alpha-actin in WT but not in KO mice. These results indicate that ET-1 is an upstream activator of NFATc3 during intermittent hypoxia, contributing to the resultant hypertension and increased wall thickness.
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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 OpenQuestion graph.