ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2023
GluA1 Degradation by Autophagy Contributes to Circadian Rhythm Effects on Cerebral Ischemia Injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- The Regulatory Role of Non-Coding RNAs in Autophagy-Dependent Ischemia-Reperfusion Injury of the Brain.Current issues in molecular biology · 2025Review
- The Use of Identified Hypoxia-related Genes to Generate Models for Predicting the Prognosis of Cerebral Ischemia‒reperfusion Injury and Developing Treatment Strategies.Molecular neurobiology · 2025Article
- Research progress on the role and mechanism of circadian clock geneFrontiers in immunology · 2025Review
- Diurnal variation in brain injury after cardiac arrest and cardiopulmonary resuscitation.Frontiers in neurology · 2025Article
- Effects of music on post-stroke sleep disorders and treatment perspectives: review and narrative synthesis.Frontiers in human neuroscience · 2025Review
- The Biological Clock of Liver Metabolism in Metabolic Dysfunction-Associated Steatohepatitis Progression to Hepatocellular Carcinoma.Biomedicines · 2024Review
- Biological and Procedural Predictors of Outcome in the Stroke Preclinical Assessment Network (SPAN) Trial.Circulation research · 2024Article
- The Role of Circadian Rhythm in Neurological Diseases: A Translational Perspective.Aging and disease · 2024Review
- Natural Compounds for Preventing Age-Related Diseases and Cancers.International journal of molecular sciences · 2024Review
- Deciphering Post-Stroke Sleep Disorders: Unveiling Neurological Mechanisms in the Realm of Brain Science.Brain sciences · 2024Review
- Salvianolic Acid B Attenuates Excitotoxic Neuronal Injury After Transient Cerebral Ischemia.In vivo (Athens, Greece)Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms of many diseases, including central nervous system disorders, are regulated by circadian rhythms. The development of brain disorders such as depression, autism, and stroke is strongly associated with circadian cycles. Previous studies have shown that cerebral infarct volume is smaller at night (active phase) than during the day (inactive phase) in ischemic stroke rodent models. However, the underlying mechanisms remain unclear. Increasing evidence suggests that glutamate systems and autophagy play important roles in the pathogenesis of stroke. Here, we report that GluA1 expression was decreased and autophagic activity was increased in active-phase male mouse models of stroke compared with the inactive-phase models. In the active-phase model, induction of autophagy decreased the infarct volume, whereas inhibition of autophagy increased the infarct volume. Meanwhile, GluA1 expression was decreased following activation of autophagy and increased following inhibition of autophagy. We used Tat-GluA1 to uncouple p62, an autophagic adapter, from GluA1 and found that this blocked the degradation of GluA1, an effect similar to that of inhibition of autophagy in the active-phase model. We also demonstrated that knock-out of the circadian rhythm gene
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