CNS Redox Homeostasis and Dysfunction in Neurodegenerative Diseases

Goldsteins, Gundars; Hakosalo, Vili; Jaronen, Merja; Keuters, Meike Hedwig; Lehtonen, Šárka; Koistinaho, Jari

doi:10.3390/antiox11020405

Cited by 16 publications

(13 citation statements)

References 183 publications

(200 reference statements)

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“…According to the bibliometric analysis, China was the major contributor in nanoscience‐ferroptosis studies, and thus the involvement of traditional Chinese medicine was expectable. Developing ferroptosis‐regulating nanomedicines for the therapy of diseases other than cancer. As a ubiquitous physiological mechanism, the ferroptosis process was involved in diverse diseases, not only tumor but also inflammatory [54], neurodegenerative [55], and cardiovascular diseases [56]. The critical role of ferroptosis in many diseases were gradually revealed.…”

Section: Resultsmentioning

confidence: 99%

Explicating the publication paradigm by bibliometric approaches: A case of interplay between nanoscience and ferroptosis

Huang

Wang

Shu

et al. 2022

Health Care Science

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Background: Ferroptosis has been widely investigated as an emerging drug target, while its combination with nanoscience provides bourgeoning application prospects. The development of ferroptosis regulating nanomedicines have attracted worldwide attentions in recent years. It would be meaningful to describe the relevant publication paradigm.Methods: Herein, a bibliometric analysis was performed using the database of Web of Science Core Collection to clarify the publication paradigm. The development of related publications in the last 6 years was described, and the revolutionary trends were figured out. Ultimately, the possible future exploration directions were proposed. Results:The bibliometric analysis of 327 documents of interest indicated that the main research focus was in multiple fields including Materials science, Science & technology, Chemistry, and Pharmacology & pharmacy. With

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Section: Resultsmentioning

confidence: 99%

Explicating the publication paradigm by bibliometric approaches: A case of interplay between nanoscience and ferroptosis

Huang

Wang

Shu

et al. 2022

Health Care Science

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“…Antioxidant therapies could help improve the unbalanced redox state and enhance the endogenous antioxidant defense system (De Lazzari et al, 2020). Despite of the widespread research about the benefits of rhodamines, further research is needed to better characterize the pharmacological, physiological, and therapeutic effects of this class of candidates in neurodegenerative diseases (Goldsteins et al, 2022).…”

Section: Discussionmentioning

confidence: 99%

5-(4-Hydroxy-3-dimethoxybenzylidene)-thiazolidinone improves motor functions and exerts antioxidant potential in hemiparkinsonian rats

Ren

Ding

Zhou

et al. 2022

Behavioural Pharmacology

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Our previous study demonstrated that 5-(4-hydroxy-3-dimethoxybenzylidene)-thiazolidinone (RD-1), one of rhodamine derivatives, significantly improves motor function in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mice model and could minimize mitochondrial impairment, which is a potential therapeutic target to slow down the dopaminergic neurodegeneration in Parkinson’s disease. To further evaluate its therapeutic and antioxidative potential in Parkinson’s disease, the current study was designed to explore the effect of RD-1 on hemiparkinsonian rats following unilateral 6-hydroxydopamine lesions. Motor functional behavioral tests, including apomorphine-induced rotational analysis and beam walking tests, were assessed. Our results showed that oral RD-1 administration for 2 weeks alleviated beam walking disability, but not the rotational behavior. Furthermore, compared to the sham group, tyrosine hydroxylase- (TH-) positive neurons in the substantia nigra pars compacta and fibers in the striatum were significantly preserved in the RD-1 treatment group. The abnormal activities of superoxide dismutase, catalase, and glutathione peroxidase and contents of MDA were evidently ameliorated by RD-1, at least partly. We conclude that RD-1 could improve motor functions and alleviate the loss of dopaminergic expression in the nigrostriatal pathway of Parkinson’s disease rats, and the protective mechanism of RD-1 against neurodegeneration was possibly via its modulation of antioxidation.

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“…Age-related changes in the Nrf2 regulatory system involve upregulation of Keap1 and Bach1, which act as repressors of Nrf2 [4,6,9,16]. Apart from increased ROS/RNS and oxidative stress, Nrf2 reduction generates a lower capacity of injury-induced neurogenesis, autophagy deregulation, and ferroptosis, among other processes [3,14,[17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Age-Dependent Changes in Nrf2/Keap1 and Target Antioxidant Protein Expression Correlate to Lipoxidative Adducts, and Are Modulated by Dietary N-3 LCPUFA in the Hippocampus of Mice

Díaz,

Valdés-Baizabal,

de Pablo

et al. 2024

Antioxidants

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The brain has a high metabolism rate that may generate reactive oxygen and nitrogen species. Consequently, nerve cells require highly efficient antioxidant defenses in order to prevent a condition of deleterious oxidative stress. This is particularly relevant in the hippocampus, a highly complex cerebral area involved in processing superior cognitive functions. Most current evidence points to hippocampal oxidative damage as a causal effect for neurodegenerative disorders, especially Alzheimer’s disease. Nuclear factor erythroid-2-related factor 2/Kelch-like ECH-associated protein 1 (Nrf2/Keap1) is a master key for the transcriptional regulation of antioxidant and detoxifying systems. It is ubiquitously expressed in brain areas, mainly supporting glial cells. In the present study, we have analyzed the relationships between Nrf2 and Keap1 isoforms in hippocampal tissue in response to aging and dietary long-chain polyunsaturated fatty acids (LCPUFA) supplementation. The possible involvement of lipoxidative and nitrosative by-products in the dynamics of the Nrf2/Keap1 complex was examined though determination of protein adducts, namely malondialdehyde (MDA), 4-hydroxynonenal (HNE), and 3-nitro-tyrosine (NTyr) under basal conditions. The results were correlated to the expression of target proteins heme-oxygenase-1 (HO-1) and glutathione peroxidase 4 (GPx4), whose expressions are known to be regulated by Nrf2/Keap1 signaling activation. All variables in this study were obtained simultaneously from the same preparations, allowing multivariate approaches. The results demonstrate a complex modification of the protein expression patterns together with the formation of adducts in response to aging and diet supplementation. Both parameters exhibited a strong interaction. Noticeably, LCPUFA supplementation to aged animals restored the Nrf2/Keap1/target protein patterns to the status observed in young animals, therefore driving a “rejuvenation” of hippocampal antioxidant defense.

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CNS Redox Homeostasis and Dysfunction in Neurodegenerative Diseases

Cited by 16 publications

References 183 publications

Explicating the publication paradigm by bibliometric approaches: A case of interplay between nanoscience and ferroptosis

Explicating the publication paradigm by bibliometric approaches: A case of interplay between nanoscience and ferroptosis

5-(4-Hydroxy-3-dimethoxybenzylidene)-thiazolidinone improves motor functions and exerts antioxidant potential in hemiparkinsonian rats

Age-Dependent Changes in Nrf2/Keap1 and Target Antioxidant Protein Expression Correlate to Lipoxidative Adducts, and Are Modulated by Dietary N-3 LCPUFA in the Hippocampus of Mice

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