ArticleJournal of inflammation research2022
Nrf2 Inhibits the Progression of Parkinson's Disease by Upregulating AABR07032261.5 to Repress Pyroptosis.
Article in Journal of inflammation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Possible Mitigating Effect of Nobiletin on Rotenone-Induced Parkinsonism in Male Albino Rat Model: Targeting Bmal1/Nrf2 Mediated Ferroptosis and Restoring Mitochondrial Mitophagy.Neurochemical research · 2025Article
- Therapeutic effect of formononetin in 6-OHDA induced Parkinson disease in rats.Inflammopharmacology · 2025Article
- Triple-Combination Therapy with a Multifunctional Yolk-Shell Nanozyme Au@CeOAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integrating bioinformatics and machine learning to uncover lncRNA LINC00269 as a key regulator in Parkinson's disease via pyroptosis pathways.European journal of medical research · 2024Article
- Tetramethylpyrazine nitrone exerts neuroprotection via activation of PGC-1α/Nrf2 pathway in Parkinson's disease models.Journal of advanced research · 2024Article
- Myricetin mitigates motor disturbance and decreases neuronal ferroptosis in a rat model of Parkinson's disease.Scientific reports · 2024Article
- Possible role of lncRNAs in amelioration of Parkinson's disease symptoms by transplantation of dopaminergic cells.NPJ Parkinson's disease · 2024Article
- Review
- The Common Denominators of Parkinson's Disease Pathogenesis and Methamphetamine Abuse.Current neuropharmacology · 2024Review
- Parkinson's disease models and death signaling: what do we know until now?Frontiers in neuroanatomy · 2024Review
- Cannabinoid type 2 receptor activation inhibits MPPMolecular biology reports · 2023Article
- Normal and Pathological NRF2 Signalling in the Central Nervous System.Antioxidants (Basel, Switzerland) · 2022Review
- Chronic Cerebral Hypoperfusion Aggravates Parkinson's Disease Dementia-Like Symptoms and Pathology in 6-OHDA-Lesioned Rat through Interfering with Sphingolipid Metabolism.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveParkinson's disease (PD) is associated with dysregulated neural cell death, such as pyroptosis, but its regulatory mechanisms are poorly understood. This study investigated roles of nuclear factor E2-related factor 2 (Nrf2) in regulating pyroptosis and PD development.
methodsCellular and rat PD models established by 6-OHDA exposure were subjected to Nrf2 overexpression. Neurobehavioral functions were assessed by the traction test, Morris Water Maze, and open field test. Cell proliferation was analyzed by MTS assay, while flow cytometry was applied to quantify levels of reactive oxygen species (ROS) and apoptosis. Nissl bodies in rat brains were detected by Nissl staining, and cell apoptosis in brain tissues was assessed by terminal deoxynucleotidyl transferase dUTP nick-end labeling. Differential expression of lncRNA and mRNA was characterized by deep sequencing.
resultsA cellular PD model was successfully established by inducing PC12 cell differentiation with nerve growth factor-β and exposing differentiated cells to 6-OHDA. Cells exhibited significantly increased ROS levels, enhanced pyroptosis, and inhibited Nrf2 phosphorylation. The rat PD model exhibited impaired muscle strength, increased pyroptosis, and repressed Nrf2 phosphorylation. Nrf2 overexpression effectively repressed pyroptosis in both cellular and rat PD models. Marked alterations of lncRNA and mRNA profiles were induced by Nrf2 overexpression in the cellular PD model, which involved multiple signaling pathways. Silencing of the lncRNA AABR07032261.5 significantly promoted pyroptosis in the cellular PD model.
conclusionNrf2 suppressed PD pathogenesis in cellular and animal models by promoting AABR07032261.5, which repressed pyroptosis.
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