ArticleInternational journal of biological sciences2026
LINC-EPS Protects Against Neurodegeneration by Driving a PGC-1α-Mediated Anti-Ferroptosis Program in Parkinson's Disease.
Article in International journal of biological sciences, 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) is a progressive neurodegenerative disorder characterized by dopaminergic (DA) neuron loss and currently lacks disease-modifying treatments. We found that the long intergenic non-coding RNA LINC-EPS was markedly reduced in peripheral blood of PD patients, correlating with greater clinical severity. Similar downregulation was observed in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) PD mice and 1-methyl-4-phenylpyridinium-treated DA neurons. Knockout of LINC-EPS, either systemically or specifically in DA neurons, aggravated motor deficits and DA neurodegeneration, whereas AAV-mediated overexpression rescued these phenotypes. LINC-EPS protected DA neurons by suppressing ferroptosis, acting as a scaffold that binds both PGC-1α protein and a T-box element in its promoter, thereby recruiting PGC-1α to enhance its own transcription through a positive feedback loop. This activation improved mitochondrial function, lowered reactive oxygen species, inhibited lipid peroxidation, and conferred ferroptosis resistance. Pharmacological activation of PGC-1α with ZLN005 rescued neurodegeneration in LINC-EPS-deficient PD mice. Our study identifies a novel LINC-EPS/PGC-1α axis that mitigates ferroptotic DA neuron loss and supports PGC-1α activation as a promising therapeutic strategy for PD progression.
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