ArticleAntioxidants & redox signaling2014
CD36 upregulation mediated by intranasal LV-NRF2 treatment mitigates hypoxia-induced progression of Alzheimer's-like pathogenesis.
Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 53 citations in OpenAlex.
- CD36 as a Context-Dependent Regulator of Metabolic Switching in Acute and Chronic Hypoxia.Biomolecules · 2026Review
- Metabolic Regulatory Networks in Ferroptosis During Alzheimer's Disease, Mechanisms of Glial Cell Action, and Pathological Correlations with Neuritic Plaques.International journal of general medicine · 2026Review
- Recent Advances in Nose-to-Brain Gene Delivery for Central Nervous System Disorders.Pharmaceutics · 2025Review
- Targeting hypoxia-related pathobiology in Alzheimer's disease: strategies for prevention and treatment.Molecular biology reports · 2025Review
- Intermittent hypoxia training enhances Aβ endocytosis by plaque associated microglia via VPS35-dependent TREM2 recycling in murine Alzheimer's disease.Alzheimer's research & therapy · 2024Article
- Omega-3 Polyunsaturated Fatty Acids in Managing Comorbid Mood Disorders in Chronic Obstructive Pulmonary Disease (COPD): A Review.Journal of clinical medicine · 2023Review
- The neuroprotective effects of oxygen therapy in Alzheimer's disease: a narrative review.Neural regeneration research · 2023Review
- Analysis of gene expression profiles in Alzheimer's disease patients with different lifespan: A bioinformatics study focusing on the disease heterogeneity.Frontiers in aging neuroscience · 2023Article
- Oxygen Sensing and Signaling in Alzheimer's Disease: A Breathtaking Story!Cellular and molecular neurobiology · 2022Review
- Microglia in the Neuroinflammatory Pathogenesis of Alzheimer's Disease and Related Therapeutic Targets.Frontiers in immunology · 2022Review
- The potential role of Keap1-Nrf2 pathway in the pathogenesis of Alzheimer's disease, type 2 diabetes, and type 2 diabetes-related Alzheimer's disease.Metabolic brain disease · 2021Review
- Optimization of 1,4-bis(arylsulfonamido)naphthalene-N,N'-diacetic acids as inhibitors of Keap1-Nrf2 protein-protein interaction to suppress neuroinflammation.Bioorganic & medicinal chemistry · 2021Article
- Review
- Protective Effects from the Ischemic/Hypoxic Stress Induced by Labor in the High-Altitude Tibetan Placenta.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Targeting Transcription Factor Nrf2 (Nuclear Factor Erythroid 2-Related Factor 2) for the Intervention of Vascular Cognitive Impairment and Dementia.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Hypoxia-Induced Neuroinflammation in Alzheimer's Disease: Potential Neuroprotective Effects ofFrontiers in physiology · 2021Review
- Liver Growth Factor "LGF" as a Therapeutic Agent for Alzheimer's Disease.International journal of molecular sciences · 2020Article
- The Activation of Phosphatidylserine/CD36/TGF-Oxidative medicine and cellular longevity · 2020Article
- The Important Interface Between Apolipoprotein E and Neuroinflammation in Alzheimer's Disease.Frontiers in immunology · 2020Review
- Plasma soluble CD36, carotid intima-media thickness and cognitive function in patients with type 2 diabetes.Archives of medical science : AMS · 2017Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThere is extensive evidence that oxidative stress induces cellular dysfunction in the brain and plays a critical role in Alzheimer's disease (AD) pathogenesis. Hypoxia increases factors involved in oxidative stress injury and contributes to the onset and progression of AD. Nuclear factor erythroid 2-related factor 2 (NRF2), a major component regulating antioxidant response, is attenuated in the AD brain. Importantly, NRF2 directly regulates the alternative first exons of CD36, an important participant in oxidative and inflammatory processes. To explore the effects of hypoxia-induced deterioration of AD-like pathogenesis and investigate the correlation between hypoxia-induced NRF2 signal alterations and CD36 expression, we examined the NRF2 signaling, CD36, and oxidative stress events in hypoxia-treated APPswe/PSEN1dE9 (APP/PS1) mice brain.
resultsWe observed that hypoxia treatment increased oxidative stress, exacerbated inflammation, and aggravated learning defects in aged APP/PS1 mice. Microglia from hypoxia-treated mice brain exhibited marked reduction in CD36 expression and inhibition of β-amyloid (Aβ) degradation. Accordingly, hypoxia treatment caused a decrease in transactivation of NRF2 target genes in the aging mouse brain. Intranasal administration with a lentiviral vector encoding human NRF2 increased CD36 expression, ameliorated the weak antioxidant response triggered by hypoxia, diminished Aβ deposition, and improved spatial memory defects. INNOVATION: In this study, we demonstrated for the first time that NRF2 intranasal treatment-induced increases of CD36 could enhance Aβ clearance in AD transgenic mouse.
conclusionThese results suggest that targeting NRF2-mediated CD36 expression might provide a beneficial intervention for cognitive impairment and oxidative stress in AD progression.
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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.