ArticleInternational journal of molecular sciences2026
Microglial Nrf2 Activation Orchestrates Ferroptosis Inhibition and α-Synuclein Clearance in Parkinson's Disease.
Article in International journal of molecular 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 pathologically characterized by the abnormal aggregation of α-synuclein and the progressive loss of dopaminergic neurons, with microglia-mediated neuroinflammation acting as a pivotal driver of pathogenesis. Ferroptosis, an iron-dependent form of regulated cell death, significantly contributes to PD progression. However, the precise mechanisms governing microglial ferroptosis under α-synuclein pathology, particularly the regulatory role of the master antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), remain elusive. Here, we employed an in vitro BV2 microglial model and an in vivo A53T transgenic mouse model to elucidate the regulatory effects and underlying mechanisms of Nrf2 on ferroptosis-associated phenotypes induced by α-synuclein pre-formed fibrils (PFFs). In vitro, PFF treatment significantly downregulated microglial Nrf2 expression, triggering ferroptosis-associated phenotypes characterized by reactive oxygen species (ROS) accumulation, ferrous iron (Fe
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