ArticleCNS neuroscience & therapeutics2026
Upregulated PKM2 Protects Dopaminergic Neurons From Oxidative Damage Through Nrf2 Transactivation in an MPTP-Induced Mouse Model of Parkinson's Disease.
Article in CNS neuroscience & therapeutics, 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
backgroundThe death of dopaminergic neurons in the substantia nigra pars compacta (SNc) is the core defining pathological change of Parkinson's disease (PD). We previously showed that reducing neuronal pyruvate kinase M2 (PKM2) aggravates oxidative damage and accelerates dopaminergic neuron loss, although the mechanism remained unclear.
methodsIn the MPTP mouse model, we evaluated antioxidant responses and neuronal survival after selectively deleting PKM2 in dopaminergic neurons or overexpressing PKM2. In MPP
resultsNeuronal PKM2 knockdown abolished MPTP-induced activation of Nrf2 target genes, exacerbated lipid peroxidation and DNA damage, and accelerated loss of dopaminergic neurons, whereas PKM2 overexpression restored the antioxidant response and mitigated neurodegeneration. Mechanistically, ROS generated by MPP
conclusionThese findings delineate a signaling pathway in which ROS elevate hnRNP A1/A2, favor PKM2 production, and activate Nrf2, thereby providing a mechanistic basis for the oxidative injury and progressive dopaminergic neuron degeneration observed with PKM2 loss. The PKM2-Nrf2 axis thus emerges as a candidate target for disease-modifying therapy in PD.
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