AI Article Synopsis
- Parkinson's disease (PD) is a common neurodegenerative disorder caused by the loss of dopamine-producing neurons, resulting in motor issues and linked to autophagy dysfunction.
- This study investigates the role of miR-214-3p in PD, finding that it hinders autophagy and leads to the death of dopaminergic neurons, worsening PD symptoms when overexpressed.
- The research also uncovers that miR-214-3p targets ATG3, highlighting its potential as a biomarker and therapeutic target to improve autophagy and protect neurons in PD.
Article Abstract
Parkinson's disease (PD) is a prevalent neurodegenerative disorder characterized by dopaminergic neuron death in the substantia nigra, leading to motor dysfunction. Autophagy dysregulation has been implicated in PD pathogenesis. This study explores the role of miR-214-3p in PD, focusing on its impact on autophagy and dopaminergic neuron viability. Using in vitro and in vivo models, we demonstrate that miR-214-3p inhibits autophagy and promotes dopaminergic neuron apoptosis. Behavioral assessments and molecular analyses reveal exacerbation of PD symptoms upon miR-214-3p overexpression. Furthermore, mechanistic investigations identify ATG3 as a target, shedding light on miR-214-3p's regulatory role in autophagy. These findings enhance our understanding of PD pathogenesis and propose miR-214-3p as a potential biomarker and therapeutic target for modulating autophagy and neuronal survival in PD.
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| http://dx.doi.org/10.1016/j.biopha.2024.116123 | DOI Listing |
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