ArticleThe Journal of physiology2018
DNA methylation in the central and efferent limbs of the chemoreflex requires carotid body neural activity.
Article in The Journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Translating physiology of the arterial chemoreflex into novel therapeutic interventions targeting carotid bodies in cardiometabolic disorders.The Journal of physiology · 2025Review
- Hypoxia sensing in the body: An update on the peripheral and central mechanisms.Experimental physiology · 2024Review
- Possible Molecular Mechanisms of Hypertension Induced by Sleep Apnea Syndrome/Intermittent Hypoxia.Life (Basel, Switzerland) · 2024Review
- Adaptive cardiorespiratory changes to chronic continuous and intermittent hypoxia.Handbook of clinical neurology · 2022Review
- Carotid body chemoreceptors: physiology, pathology, and implications for health and disease.Physiological reviews · 2021Review
- Intermittent Hypoxia-Induced Activation of Endothelial Cells Is MediatedFrontiers in physiology · 2021Article
- Hypoxia-inducible factors and obstructive sleep apnea.The Journal of clinical investigation · 2020Review
- The Carotid Body a Common Denominator for Cardiovascular and Metabolic Dysfunction?Frontiers in physiology · 2020Review
- Pre- and post-inspiratory neurons change their firing properties in female rats exposed to chronic intermittent hypoxia.Neuroscience · 2019Article
- Neural Activation of Molecular Circuitry in Intermittent Hypoxia.Current opinion in physiology · 2019Article
- Rostral Ventrolateral Medulla and Hypertension.Hypertension (Dallas, Tex. : 1979) · 2018Review
- Advances in cellular and integrative control of oxygen and carbon dioxide homeostasis.The Journal of physiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
key pointsThe mechanisms underlying long-term (30 days) intermittent hypoxia (LT-IH)-evoked DNA methylation of anti-oxidant enzyme (AOE) gene repression in the carotid body (CB) reflex pathway were examined. LT-IH-treated rats showed increased reactive oxygen species (ROS) levels in the CB reflex pathway. Administration of a ROS scavenger or CB ablation blocked LT-IH-evoked DNA methylation and AOE gene repression in the central and efferent limbs of the CB reflex. LT-IH increased DNA methyltransferase (Dnmt) activity through upregulation of Dnmt1 and 3b proteins by ROS-dependent inactivation of glycogen synthase kinase 3β (GSK3β) by Akt. A pan-Akt inhibitor prevented LT-IH-induced GSK3β inactivation, elevated Dnmt protein expression and activity, AOE gene methylation, sympathetic activation and hypertension. ABSTRACT: Long-term exposure to intermittent hypoxia (LT-IH; 30 days), simulating blood O
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.