High Glucose Aggravates Cerebral Ischemia/Reperfusion via Truncated NLRP3-Mediated Hexokinase-2 Translocation.

ABSTRACT:

Background

High blood glucose is a well-established risk factor for poor outcomes in ischemic stroke. However, the underlying molecular mechanisms linking high blood glucose to worsened stroke outcomes remain unclear.

Objectives

Previous studies have implicated the NLRP3 inflammasome, a key mediator of neuroinflammation, in cerebral ischemia/reperfusion (I/R) injury. Under high blood glucose conditions, NLRP3 activation is amplified, potentially driving a vicious cycle of inflammation and neuronal death. Yet, how high blood glucose specifically modulates NLRP3 activation and its downstream pathways remains unclear. This study aimed to investigate the specific mechanisms by which high glucose enhances NLRP3 inflammasome activity and contributes to worsened brain injury follow

SUBMITTER: Zhang H 

PROVIDER: S-EPMC12627235 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature