bioRxiv / medRxiv
open access
Nrf2 regulates ICAM-1-mediated neutrophil extracellular trap formation after traumatic brain injury.
Traumatic brain injury (TBI) triggers secondary neurovascular damage characterized by oxidative stress, blood-brain barrier (BBB) disruption, and neuroinflammation, leading to long-term cognitive deficits. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a master regulator of cellular antioxida
Conceptio Open Archive
Analyze & explore related research in Conceptio
Connect this record directly into your research workflow or AI agent. Explore citations across open repositories, query full text, and export structured proof bundles.
This document is indexed with metadata only: full text is not available in the archive for this record. Open the official source ↗
Related documents
- The role of NRF2 transcription factor in inflammatory skin diseases#374601
- HIPPOCAMPAL CIRCUIT ALTERATIONS AND MICROGLIAL CONTRIBUTIONS TO LEARNING AND MEMORY DYSFUNCTIONS FOLLOWING MILD TRAUMATIC BRAIN INJURY#929479
- NF-κB as a therapeutic target of rheumatoid arthritis#70029
- Analysis of homozygous and heterozygous Csf1r knockout in the rat as a model for understanding microglial function in brain development and the impacts of human CSF1R mutations#1312619
- FPR2 deficiency alleviates LPS-induced depressive-like behaviors in mice by suppressing the microglial CSF1/NLRP3 inflammasome pathway.#1330060
Record · ID 1336104
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Bring this data into your agent: Connect via MCP or API · 20 free credits to start · no card required
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive