ArticleiScience2025
Nrf2 controls homeostatic transcriptional signatures and inflammatory responses in a cell-type specific manner in the adult mouse brain.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Review
- Nrf2 modulates cytosolic and mitochondrial calcium signal.Redox biology · 2026Article
- Neuronal overexpression of Nrf2 reduces dystrophic neurites in 5XFAD Alzheimer's disease model mice.Alzheimer's research & therapy · 2026Article
- Neuronal overexpression of Nrf2 reduces dystrophic neurites in 5XFAD Alzheimer's disease model mice.bioRxiv : the preprint server for biology · 2026Article
- The electrophilic metabolite of kynurenine, kynurenine-CKA, targets C151 in Keap1 to derepress Nrf2.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nrf2 is a promising therapeutic target for neurological disorders, but its mechanisms of action remain unclear. While often linked to anti-inflammatory effects, this is mostly based on studies involving pharmacological activation. In the brain, Nrf2 is highly expressed in microglia, astrocytes, and endothelial cells. As yet, the brain cell type-specific role of Nrf2 in regulating the basal transcriptome and controlling neuroinflammation is unknown. To address this, we employed three inducible conditional Nrf2 knockout mice in which Nrf2 is deleted in microglia, astrocytes, and brain endothelial cells, respectively. We discovered that in healthy brains, Nrf2 controls distinct transcriptional profiles in the three brain cell types under study. Surprisingly, after systemic inflammation, microglia, and astrocytes lacking Nrf2 showed reduced inflammatory responses, unlike endothelial cells. Additionally, even without any insult, Nrf2 in microglia supported the expression of pro-inflammatory genes. Our findings reveal a pro-inflammatory role for endogenous Nrf2 in specific brain cell types.
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