ReviewFrontiers in physiology2018
Contribution of Oxidative Stress and Inflammation to the Neurogenic Hypertension Induced by Intermittent Hypoxia.
Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Lung Vascular Remodeling and Oxidative Damage Induced by Chronic Intermittent Hypoxia.International journal of molecular sciences · 2026Article
- Development and Validation of an Explainable Machine Learning Model for Identifying Hypertension Status in Patients With Obstructive Sleep Apnea.Journal of clinical hypertension (Greenwich, Conn.) · 2026Article
- ZEB1 and Neural Stem Cells: Insights into Microglia-Conditioned Medium-Driven Neuroinflammation.Cells · 2025Article
- Predictor and prognostic modeling in cardiorenal syndrome type 2: a retrospective study of multicenter.Biomarkers in medicine · 2025Article
- Sleep-Disordered Breathing and Central Respiratory Control in Children: A Comprehensive Review.Children (Basel, Switzerland) · 2025Review
- Cluster Headache and Hypoxia: Breathing New Life into an Old Theory, with Novel Implications.Neurology international · 2024Review
- Effect of aortic smooth muscle BK channels on mediating chronic intermittent hypoxia-induced vascular dysfunction.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- The association between flavonoids intake and hypertension in U.S. adults: A cross-sectional study from The National Health and Nutrition Examination Survey.Journal of clinical hypertension (Greenwich, Conn.) · 2024Article
- Intermittent hypoxia induces Th17/Treg imbalance in a murine model of obstructive sleep apnea.PloS one · 2024Article
- The effect of microvascular decompression of the CN IX-X root entry/exit zone and the ventrolateral medulla in neurogenic hypertension involving the vertebral/basilar artery.Frontiers in neurology · 2024Article
- Chemogenetic inhibition of NTS astrocytes normalizes cardiac autonomic control and ameliorate hypertension during chronic intermittent hypoxia.Biological research · 2023Article
- Obstructive Sleep Apnea and Venous Thromboembolism: Unraveling the Emerging Association.Cureus · 2023Review
- Neurogenic Hypertension, the Blood-Brain Barrier, and the Potential Role of Targeted Nanotherapeutics.International journal of molecular sciences · 2023Review
- Sulforaphane Attenuates Chronic Intermittent Hypoxia-Induced Brain Damage in MiceFrontiers in cellular neuroscience · 2022Article
- Unlocking mammalian regeneration through hypoxia inducible factor one alpha signaling.Biomaterials · 2021Review
- Ketogenic diet effects on inflammatory allodynia and ongoing pain in rodents.Scientific reports · 2021Article
- Immunity and the carotid body: implications for metabolic diseases.Bioelectronic medicine · 2020Review
- Exploring the Mediators that Promote Carotid Body Dysfunction in Type 2 Diabetes and Obesity Related Syndromes.International journal of molecular sciences · 2020Review
- Article
- Upregulating Nrf2 in the RVLM ameliorates sympatho-excitation in mice with chronic heart failure.Free radical biology & medicine · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic intermittent hypoxia (CIH), the hallmark of obstructive sleep apnea, is the main risk factor to develop systemic hypertension. Oxidative stress, inflammation, and sympathetic overflow have been proposed as possible mechanisms underlying the CIH-induced hypertension. CIH potentiates the carotid body (CB) chemosensory discharge leading to sympathetic overflow, autonomic dysfunction, and hypertension. Oxidative stress and pro-inflammatory molecules are involved in neurogenic models of hypertension, acting on brainstem and hypothalamic nuclei related to the cardiorespiratory control, such as the nucleus of the solitary tract, which is the primary site for the afferent inputs from the CB. Oxidative stress and pro-inflammatory molecules contribute to the activation of the CB chemoreflex pathway in CIH-induced hypertension. In this brief review, we will discuss new evidence for a critical role of oxidative stress and neuro-inflammation in development of the CIH-induced hypertension through activation of the CB chemoreflex 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.