ArticleSleep & breathing = Schlaf & Atmung2017
The role of the Nox4-derived ROS-mediated RhoA/Rho kinase pathway in rat hypertension induced by chronic intermittent hypoxia.
Article in Sleep & breathing = Schlaf & Atmung, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Repositioning Perindopril for Mitigation of Methotrexate-Induced Hepatotoxicity in Rats.Pharmaceuticals (Basel, Switzerland) · 2025Article
- RhoA/ROCK1 regulates the mitochondrial dysfunction through Drp1 induced by Porphyromonas gingivalis in endothelial cells.Journal of cellular and molecular medicine · 2023Article
- Advances in Molecular Pathology of Obstructive Sleep Apnea.Molecules (Basel, Switzerland) · 2022Review
- Fasudil Ameliorates Methotrexate-Induced Hepatotoxicity by Modulation of Redox-Sensitive Signals.Pharmaceuticals (Basel, Switzerland) · 2022Article
- NADPH oxidase family proteins: signaling dynamics to disease management.Cellular & molecular immunology · 2022Review
- LncRNA FENDRR Servers as a Possible Marker of Essential Hypertension and Regulates Human Umbilical Vein Endothelial Cells Dysfunction via miR-423-5p/Nox4 Axis.International journal of general medicine · 2022Article
- NOX4, MDA, IMA and oxidative DNA damage: can these parameters be used to estimate the presence and severity of OSA?Sleep & breathing = Schlaf & Atmung · 2021Article
- Salidroside Ameliorated Intermittent Hypoxia-Aggravated Endothelial Barrier Disruption and AtherosclerosisFrontiers in pharmacology · 2021Article
- Review - Nutraceuticals Can Target Asthmatic Bronchoconstriction: NADPH Oxidase-Dependent Oxidative Stress, RhoA and Calcium Dynamics.Journal of asthma and allergy · 2021Review
- Article
- Sodium Tanshinone II Sulfonate A Ameliorates Hypoxia-Induced Pulmonary Hypertension.Frontiers in pharmacology · 2020Article
- Sensory plasticity of carotid body is correlated with oxidative stress in paraventricular nucleus during chronic intermittent hypoxia.Journal of cellular physiology · 2019Article
- RhoGTPase in Vascular Disease.Cells · 2019Review
- Toll-like receptor-4 deficiency alleviates chronic intermittent hypoxia-induced renal injury, inflammation, and fibrosis.Sleep & breathing = Schlaf & Atmung · 2019Article
- Is Aberrant Reno-Renal Reflex Control of Blood Pressure a Contributor to Chronic Intermittent Hypoxia-Induced Hypertension?Frontiers in physiology · 2019Review
- The role of NF-κB-mediated JNK pathway in cognitive impairment in a rat model of sleep apnea.Journal of thoracic disease · 2018Article
- DL-Propargylglycine protects against myocardial injury induced by chronic intermittent hypoxia through inhibition of endoplasmic reticulum stress.Sleep & breathing = Schlaf & Atmung · 2018Article
- Cardiac pathophysiology in response to environmental stress: a current review.Current opinion in physiology · 2018Article
- The Importance of NADPH Oxidases and Redox Signaling in Angiogenesis.Antioxidants (Basel, Switzerland) · 2017Review
- Establishment of a Rabbit Model of Chronic Obstructive Sleep Apnea and Application in Cardiovascular Consequences.Chinese medical journal · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundObstructive sleep apnea syndrome, which is a risk factor for resistant hypertension, is characterized by chronic intermittent hypoxia (CIH) and is associated with many cardiovascular diseases. CIH elicits systemic oxidative stress and sympathetic hyperactivity, which lead to hypertension. Rho kinases (ROCKs) are considered to be major effectors of the small GTPase RhoA and have been extensively studied in the cardiovascular field. Upregulation of the RhoA/ROCK signaling cascade is observed in various cardiovascular disorders, such as atherosclerosis, pulmonary hypertension, and stroke. However, the exact molecular function of RhoA/ROCK in CIH remains unclear and requires further study.
objectiveThis study aimed to investigate the role of the NADPH oxidase 4 (Nox4)-induced ROS/RhoA/ROCK pathway in CIH-induced hypertension in rats.
methodsMale Sprague-Dawley rats were exposed to CIH for 21 days (intermittent hypoxia of 21% O
resultsCompared with the BP of RA rats, the BP of CIH-V rats started to increase 2 weeks after the beginning of the experiment, subsequently stabilizing at a high level at the end of the third week. CIH increased both RSNA and oxidative stress. This response was attenuated by treatment of the rats with GKT137831 or NAC. Inhibiting Nox4 activity or ROS production reduced RhoA/ROCK expression. Treatment with Y27632 reduced both BP and RSNA in rats exposed to CIH.
conclusionHypertension can be induced by CIH in SD rats. The CIH-induced elevation of BP is at least partially mediated via the Nox4-induced ROS/RhoA/ROCK pathway.
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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.