miR-214-3p promotes the pathogenesis of Parkinson's disease by inhibiting autophagy

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. [Display omitted] •MiR-214-3p is significantly up-regulated both in PD cell model and animal model.•Overexpression of miR-214-3p inhibits dopaminergic neurons’ activity and autophagy.•Overexpression of ATG3 counteracts the regulation effect of miR-214-3p.