ArticleJournal of neuroinflammation2025
Repurposing of epalrestat for neuroprotection in parkinson's disease via activation of the KEAP1/Nrf2 pathway.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Neuroprotective Mechanisms of Paeoniflorin in Parkinson's Models: Involvement of BDNF-Dependent PI3K/Akt and ERK/CREB Pathways.Current issues in molecular biology · 2026Article
- Decode the Ubiquitinome in Parkinson's Disease: From Pathological Aggregates to Targeted DUB Therapeutics.Neuroscience bulletin · 2026Review
- Nrf2 Activators in Parkinson's Disease: Modulating Mitophagy and Regulating Cuproptosis.Molecular neurobiology · 2026Review
- Engineered neuronal exosomes mediate α-synuclein clearance to ameliorate Parkinson's disease.Journal of nanobiotechnology · 2026Article
- Systematic Evaluation of a Mouse Model of Aging-Associated Parkinson's Disease Induced with MPTP and D-Galactose.Biology · 2026Article
- A network-driven computational framework for identifying FDA-approved drug repurposing across heterogeneous brain cancers.Frontiers in molecular biosciences · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundEpalrestat (EPS), an aldose reductase inhibitor, is used to alleviate peripheral nerve disorder of diabetic patients in clinical therapy. Even though EPS exerted effects in central nervous system diseases, the neuroprotection and underlying molecular mechanism in neurodegenerative diseases, especially Parkinson's disease (PD), remains obscure. Our study aimed to investigate the potential of EPS suppressed PD progression both in vivo and in vitro.
methodsWe used 1-methyl-4-phenylpyridillium ion (MPP
resultsWe found that EPS exhibited potent antiparkinsonian activity in PD models both in vivo and in vitro. PD models treated with EPS manifested alleviated oxidative stress and mitochondrial dysfunction. Furthermore, we found EPS activated the Nrf2 signaling pathway which contributed to DAergic neurons survival in PD models. Particularly, we firstly confirmed that EPS competitively binds to KEAP1 and enhanced its degradation, thereby activating the Nrf2 signaling pathway.
conclusionsCollectively, EPS attenuates oxidative stress and mitochondrial dysfunction by directly binding KEAP1 to activate the KEAP1/Nrf2 signaling pathway, further reducing DAergic neurons damage. These findings suggest that EPS has great potential to become a therapeutic for PD as a clinically effective and safe medicine.
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