TRIM21 Exacerbates Ischemic Brain Injury by Promoting Astrocyte-Mediated Neuroinflammation via K63-Linked Ubiquitination of MDA5 - PubMed
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- #ischemic stroke
- #TRIM21
- #neuroinflammation
- TRIM21 is up-regulated in astrocytes during ischemic brain injury.
- TRIM21 deficiency reduces cerebral ischemia/reperfusion injury by decreasing inflammation and oxidative stress.
- TRIM21 interacts with MDA5, promoting its K63-linked ubiquitination and stabilization, which activates the NF-κB pathway in astrocytes.
- Overexpression of MDA5 reverses the protective effects of TRIM21 deficiency.
- Targeted silencing of TRIM21 in the brain significantly improves outcomes after cerebral ischemia/reperfusion injury.
- TRIM21 is identified as a key mediator of neuroinflammation in ischemic stroke and a potential therapeutic target.