ArticleExperimental brain research2026
miR-214-3p exacerbates mitochondrial dysfunction in parkinson's disease: a multi-omics and mechanistic study.
Article in Experimental brain research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Parkinson’s disease (PD) involves the loss of dopaminergic neurons, and prodromal PD exhibits elevated miR-214-3p, suggesting its role as a biomarker and pathogenic factor. This study investigated miR-214-3p’s effects on mitochondrial function in dopaminergic SH-SY5Y cells and mouse primary cortical neurons. In SH-SY5Y cells, proteomic/transcriptomic analyses and target prediction confirmed GFM1 as a direct target of miR-214-3p. miR-214-3p upregulation downregulated GFM1, causing severe mitochondrial bioenergetic impairment: increased reactive oxygen species (ROS), reduced oxygen consumption, diminished ATP production, and decreased respiratory chain complexes (RCC) I/IV expression. Critically, restoring GFM1 reversed these mitochondrial deficits and neuronal dysfunction. In mouse primary cortical neurons, miR-214-3p overexpression also impaired RCC I/IV but did not affect GFM1, revealing a cell type-dependent regulatory mechanism. These findings demonstrate that elevated miR-214-3p impairs mitochondrial function in a cell-specific manner. In dopaminergic cells, this damage is mediated by GFM1 downregulation, highlighting the miR-214-3p/GFM1 axis as a potential cell-type specific therapeutic target for PD and related dopaminergic neuronopathies.
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