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Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation
Microglial NLRC5 may cause lysosome problems that block cell cleanup and increase brain inflammation after stroke
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Abstract
expression was upregulated in the ischemic penumbra of mouse models and postmortem brain tissues from stroke patients.
- Increased NLRC5 levels were found in activated microglia after ischemic stroke.
- Deletion of NLRC5 in microglia resulted in significantly improved neurological outcomes and reduced brain damage in mice.
- NLRC5 induction by various stimuli led to increased release of pro-inflammatory cytokines and neurotoxicity from microglia.
- NLRC5 disrupted lysosomal function, which is crucial for the degradation of proteins and cellular debris.
- The interaction between NLRC5 and ISG15 prevented ISG15 from being degraded by , contributing to inflammation.
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Key numbers
17×
Infarct Volume Reduction
Comparison of infarct volumes in mCKO mice vs. control mice post-stroke.
28
Survival Rate Improvement
Survival rate of mCKO mice compared to control mice after tMCAO.
4
Pro-inflammatory Cytokine Reduction
Reduction in TNF-α and IL-6 levels in mCKO mice compared to controls.