ArticleNeurochemical research2023
TGF-β3 Protects Neurons Against Intermittent Hypoxia-Induced Oxidative Stress and Apoptosis Through Activation of the Nrf-2/KEAP1/HO-1 Pathway via Binding to TGF-βRI.
Article in Neurochemical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Exosomal LncRNA MALAT1 Derived from Hepatocytes in Nonalcoholic Fatty Liver Disease Regulates the miR-579-3p/Keap1/Nrf2 Pathway to Exacerbate Obstructive Sleep Apnea Syndrome.Molecular biotechnology · 2026Article
- Transcutaneous Auricular Vagus Nerve Stimulation Alleviates Oxidative Stress and Improves Neurological Outcomes After Traumatic Brain Injury in Mice.CNS neuroscience & therapeutics · 2026Article
- Mechanisms underlying end-organ injury in sleep apnoea.The European respiratory journal · 2026Review
- Identification and validation of oxidative stress-related genes in biliary atresia.Pediatric surgery international · 2025Article
- Intermittent Hypoxia Impairs Cognitive Function and Promotes Mitophagy and Lysophagy in Obstructive Sleep Apnea-Hypopnea Syndrome Rat Model.Molecular biotechnology · 2025Article
- The Protective Role of Leptin in Neurological Damage Induced by Chronic Intermittent Hypoxia.Molecular neurobiology · 2025Article
- Programmed cell death in the cognitive impairment of obstructive sleep apnea.Cell & bioscience · 2025Review
- Clinical significance of serum interleukin-4, interleukin-12, interleukin-13, and transforming growth factor-β levels in children with sleep-disordered breathing.American journal of translational research · 2025Article
- Role of Oxidative Stress in the Occurrence and Development of Cognitive Dysfunction in Patients with Obstructive Sleep Apnea Syndrome.Molecular neurobiology · 2024Review
- Impact of Chronic Intermittent Hypoxia on Cognitive Function and Hippocampal Neurons in Mice: A Study of Inflammatory and Oxidative Stress Pathways.Nature and science of sleep · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Intermittent hypoxia (IH) is the primary pathological manifestation of obstructive sleep apnea (OSA) and the main cause of OSA-induced cognitive impairment. Hippocampal neurons are considered to be critical cells affected by IH. Transforming growth factor-β3 (TGF-β3) is a cytokine with a neuroprotective effect, which plays a crucial role in resisting hypoxic brain injury, while its role in IH-induced neuronal injury is still unclear. Here, we aimed to clarify the mechanism of TGF-β3 protecting IH-exposed neurons by regulating oxidative stress and secondary apoptosis. Morris water maze results revealed that IH exposure was unable to affect the vision and motor ability of rats, but significantly affected their spatial cognition. Second-generation sequencing (RNA-seq) and subsequent experiments supported that IH decreased TGF-β3 expression and stimulated reactive oxygen species (ROS)-induced oxidative stress and apoptosis in rat hippocampus. In vitro, IH exposure significantly activated oxidative stress within HT-22 cells. Exogenous administration of Recombinant Human Transforming Growth Factor-β3 (rhTGF-β3) prevented ROS surge and secondary apoptosis in HT-22 cells caused by IH, while TGF-β type receptor I (TGF-βRI) inhibitor SB431542 blocked the neuroprotective effect of rhTGF-β3. Nuclear factor erythroid 2-related factor 2 (Nrf-2) is a transcription factor preserving intracellular redox homeostasis. rhTGF-β3 improved the nuclear translocation of Nrf-2 and activated downstream pathway. However, Nrf-2 inhibitor ML385 suppressed the activation of the Nrf-2 mechanism by rhTGF-3 and restored the effects of oxidative stress damage. These results indicate that TGF-β3 binding to TGF-βRI activates the intracellular Nrf-2/KEAP1/HO-1 pathway, reduces ROS creation, and attenuates oxidative stress and apoptosis in IH-exposed HT-22 cells.
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