ArticlePloS one2017
Monoamine oxidase A upregulated by chronic intermittent hypoxia activates indoleamine 2,3-dioxygenase and neurodegeneration.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Cerebral oxidative stress, inflammation and apoptosis induced by intermittent hypoxia: a systematic review and meta-analysis of rodent data.European respiratory review : an official journal of the European Respiratory Society · 2024Pooled it
- Sleep, Neural Circulatory Control, and Cardiovascular Disease: A Mechanistic Review.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Gut microbiota-derived tryptophan metabolites: molecular mechanisms, nutritional strategies and implications for swine health.Frontiers in veterinary science · 2026Review
- Monoamine oxidases are mediators of oxidative stress in human varicose Veins: interactions with obesity, inflammation, and angiotensin II.Molecular and cellular biochemistry · 2026Article
- Hypoxia-Induced Gut-Brain Axis Remodeling and Insomnia: Mechanisms and Microbiota Adaptive Regulation from a Translational Perspective.Journal of inflammation research · 2026Review
- Unveiling the Potential Role of Cathinone and Cathine Compounds in Alzheimer's Disease: Predictive Insights.Current Alzheimer research · 2025Article
- Nocturnal hypoxia in patients with sleep disorders: exploring its role as a mediator between neurotic personality traits and psychological symptoms.Frontiers in psychiatry · 2024Article
- Brain Iron Homeostasis and Mental Disorders.Antioxidants (Basel, Switzerland) · 2023Review
- Comparison of Monoamine Oxidase-A, Aβ Plaques, Tau, and Translocator Protein Levels in Postmortem Human Alzheimer's Disease Brain.International journal of molecular sciences · 2023Article
- (Molecules (Basel, Switzerland) · 2023Article
- Brain injury and inflammation genes common to a number of neurological diseases and the genes involved in the genesis of GABAnergic neurons are altered in monoamine oxidase B knockout mice.Brain research · 2022Article
- Intermittent Hypoxia causes targeted disruption to NMDA receptor dependent synaptic plasticity in area CA1 of the hippocampus.Experimental neurology · 2021Article
- Sex-based changes in rat brain serotonin and behavior in a model of altitude-related vulnerability to treatment-resistant depression.Psychopharmacology · 2021Article
- Daphnetin, a natural coumarin averts reserpine-induced fibromyalgia in mice: modulation of MAO-A.Experimental brain research · 2021Article
- Skimmetin/osthole mitigates pain-depression dyad via inhibiting inflammatory and oxidative stress-mediated neurotransmitter dysregulation.Metabolic brain disease · 2021Article
- Signs of Chronic Hypoxia Suggest a Novel Pathophysiological Event in α-Synucleinopathies.Movement disorders : official journal of the Movement Disorder Society · 2020Article
- Metoprolol prevents neuronal dendrite remodeling in a canine model of chronic obstructive sleep apnea.Acta pharmacologica Sinica · 2020Article
- HgS Inhibits Oxidative Stress Caused by Hypoxia through Regulation of 5-HT Metabolism Pathway.International journal of molecular sciences · 2019Article
- Comorbidity of Pain and Depression in a Lumbar Disc Herniation Model: Biochemical Alterations and the Effects of Fluoxetine.Frontiers in neurology · 2019Article
- Hypoxia Inducible Factor 1α Inhibits the Expression of Immunosuppressive Tryptophan-2,3-Dioxygenase in Glioblastoma.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Co-morbid depression is prevalent in patients with obstructive sleep apnea. Here we report that monoamine oxidase A (MAO-A) plays pathogenic roles in the comorbidity. We found that chronic intermittent hypoxia significantly increased the MAO-A expression in the rat hippocampus and markedly decreased the dendritic length and spine density in the pyramidal neurons with less pre- and post-synaptic proteins. The MAO-A upregulation resulted in increased 5-hydroxyindoleacetic acid/serotonin ratio, oxidative stress, leading to NF-κB activation, inflammation and apoptosis. Also, the expression of cytokine-responsive indoleamine 2,3-dioxygenase-1 (IDO-1) was significantly augmented in hypoxia, resulting in increased kynurenine/tryptophan ratio and lowered serotonin level in the hippocampus. Moreover, depressive-like behaviors were observed in the hypoxic rat. Administration of M30, a brain-selective MAO-A inhibitor with iron-chelating properties, prior to hypoxic treatment prevented the aberrant changes in the hippocampus and depressive behavior. In human SH-SY5Y cells expressing MAO-A but not MAO-B, hypoxia significantly increased the MAO-A expression, which was blocked by M30 or clorgyline. Collectively, the MAO-A upregulation induced by chronic intermittent hypoxia plays significant pathogenic role in oxidative stress, inflammation and IDO-1 activation resulting in serotonin depletion and neurodegeneration.
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