ArticleNPJ Parkinson's disease2025
Rotenone induced acute miRNA alterations in extracellular vesicles produce mitochondrial dysfunction and cell death.
Article in NPJ Parkinson's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Rotenone-induced oxidative stress triggers peroxisomal alterations in BV-2 microglial cells.Frontiers in cellular neuroscience · 2026Article
- Extracellular RNAs as Messengers and Early Biomarkers in Neurodegeneration.International journal of molecular sciences · 2025Review
- Activation of toll‑like receptors by non‑coding RNAs and their fragments (Review).Molecular medicine reports · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
How extracellular vesicles (EVs) may contribute to mechanisms of primary intracellular pathogenesis in Parkinson's disease (PD) remains unknown. To critically advance our understanding of how EVs influence early-stage PD pathogenesis, we tested the hypothesis that rats acutely exposed to the PD neurotoxin rotenone would produce differential miRNAs in CSF/serum-derived EVs and that such modulation would be responsible for PD-relevant functional alterations in recipient neuronal cells. We discovered that acute rotenone treatment produced significant and specific serum miRNA alterations. Primary midbrain neurons treated with serum EVs from rotenone-exposed rats produced oxidative stress, mitochondrial toxicity, and cell loss in neuronal culture. These mechanisms were dependent on miR-30a-5p and miR-484. Thus, this study has elucidated that differential expression of miRNAs in circulating EVs from serum/CSF of rats is a potential early diagnostic marker for PD, and that the modulation of cellular functions and viability due to extracellular vesicles determines the pathological fate.
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