ArticleiScience2025
Endothelial cell Nrf2 controls neuroinflammation following a systemic insult.
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.
- Engineered Small Extracellular Vesicles Targeting Tumor-Associated Endothelial Cells to Effectively Remodel the Glioma Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Attenuation of cerebral ischemia-reperfusion induced neurotoxicity by telmisartan, ertugliflozin, and omaveloxolone through Nrf2/HO-1 pathway modulation: In vivo and in silico insights.Toxicology reports · 2025Article
- Article
- Alzheimer's Disease Pathogenic Mechanisms: Linking Redox Homeostasis and Mitochondria-Associated Metabolic Pathways Through Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2).Antioxidants (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic inflammation can lead to neuroinflammation with acute consequences such as delirium and long-lasting deleterious effects including cognitive decline and the exacerbation of neurodegenerative disease progression. Here, we show that transcription factor Nrf2 controls brain endothelial cell homeostasis and barrier strength. We found that peripheral inflammation caused infiltration of macrophages, microglial activation, and inflammatory reactive astrogliosis, all of which could be prevented by RTA-404, an activator of the transcription factor Nrf2 and close structural relative of the recently FDA-approved Nrf2 activator RTA-408 (omaveloxolone). To identify the key cellular mediator(s), we generated an endothelial cell-specific Nrf2 knockout mouse. Strikingly, the effects of RTA-404 on brain endothelial activation and downstream neuroinflammatory events were abolished by endothelial cell-specific Nrf2 deletion. This places endothelial cell Nrf2 as a peripherally accessible therapeutic target to reduce the CNS-adverse consequences of systemic inflammation.
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Registered trials
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