ArticleFrontiers in aging neuroscience2025
MFN2-a multifaceted guardian against Parkinson's pathophysiology: mitochondria, ferroptosis, inflammation and oxidative stress.
Article in Frontiers in aging neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Review
- Research on the imbalance of metal homeostasis and ferroptosis mechanisms in neurodegenerative diseases.Global medical genetics · 2026Article
- Ferroptosis-induced immune modulation: a new frontier in glioblastoma therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
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Authors and funding
8 authors.
Funding
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Abstract
Background: Parkinson's disease (PD) is the second most prevalent neurodegenerative disease worldwide and its exact pathogenesis remains unclear. This study aims to comprehensively explore the role of MFN2 in PD based on Methods: Results: In PD models, the expressions of DHODH, MFN1, MFN2, GPX4, and FSP1 were significantly down-regulated, and their motor coordination, self-cognitive behavior, and exploration ability were decreased. Concurrently, inflammatory and oxidative stress responses were enhanced, cell viability was weakened, apoptosis was increased, and mitochondrial abnormalities were observed. Overexpression of MFN2 improved the motor, cognitive and neurological damage in mice, enhanced cell viability, inhibited apoptosis, reduced the levels of inflammatory and oxidative stress factors, and up-regulated the expressions of DHODH, MFN1, GPX4 and FSP1. Mitochondrial morphological observation showed that MFN2 overexpression alleviated mitochondrial abnormalities. Conclusion: MFN2 may play a protective role in PD by regulating mitochondrial function, ferroptosis, inflammation and oxidative stress-related factors, providing a new theoretical basis and potential therapeutic targets for the treatment of PD.
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