ArticleMolecular neurobiology2026
Mitochondrial Dynamics-Related Gene Regulation by Epigenetic Suppression of GCN5 Exerts Neuroprotective Effects in Rotenone-Induced Parkinson's Disease Model.
Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Review
- Advancing the frontiers of phytotherapy: a comprehensive review of botanical interventions targeting mitochondrial quality control to ameliorate endometriosis.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuron loss and mitochondrial dysfunction. Recent studies implicate the histone acetyltransferase GCN5 in regulating mitochondrial homeostasis and oxidative stress. This study investigated the therapeutic potential of GCN5 silencing via systemically administered siRNA-loaded niosomes in a rotenone-induced rat model of PD. Niosomes were prepared using the thin-film hydration method, and the most effective siRNA sequence was selected through real time quantitative PCR (RT-qPCR) and immunofluorescence in primary mesencephalic neurons. Adult male rats were divided into four groups (n = 24/group), and PD was induced with rotenone (2 mg/kg/day, s.c., for 35 days). Behavioral assessments, biochemical analyses, IVIS imaging, histopathology, immunohistochemistry, and RT-qPCR were conducted. IVIS confirmed brain accumulation of siRNA-niosomes within 3-5 h post-injection. GCN5 siRNA treatment significantly improved locomotor activity (p < 0.05), decreased MDA levels (p < 0.05), and restored SOD and dopamine levels (p < 0.05). Molecular findings showed decreased GCN5 and mitochondrial fission-related gene Drp-1 expression, increased expression of mitophagy and biogenesis markers (↑Parkin, ↑PINK1, ↑Mfn2, ↑PGC-1α), elevated TH expression, and reduced α-synuclein accumulation. Histological analysis revealed preserved midbrain cytoarchitecture and reduced neuronal damage. In conclusion, these findings highlight that epigenetic silencing of GCN5 via siRNA-loaded niosomal delivery provides neuroprotection in PD by modulating the expression of genes involved in mitochondrial dynamics, offering preclinical support for its development as a novel therapeutic strategy.
Indexed as
Identifiers
41565897What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.