Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation.

ABSTRACT:

Background

Ischemic stroke triggers excessive microglial activation and sustained neuroinflammation, driving secondary neuronal injury. Recent evidence suggests that dysfunction of the autophagy-lysosome system may be a crucial factor sustaining microglial pro-inflammatory responses, yet the underlying regulatory mechanisms remain unclear. NOD-like receptor family caspase recruitment domain-containing protein 5 (NLRC5) has been widely studied in various immune and inflammatory diseases and exhibits functional heterogeneity under different pathological conditions. However, the role of NLRC5 in modulating post-stroke neuroinflammation remains unclear.

Methods

NLRC5 expression and localization was examined in a mouse transient middle cerebral artery occlusion (tMCAO) model and

SUBMITTER: Xu S 

PROVIDER: S-EPMC12577297 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature