Transcriptional and neuroprotective effects of hexokinase-2 inhibitors administered after stroke.

ABSTRACT:

Background

The delayed inflammatory response induced by stroke can cause secondary injury to peri-infarct tissue. Microglia and other immune cells that mediate this injury require increased glycolytic flux for pro-inflammatory activation. These cells, unlike neurons, astrocytes, and most other cell types, utilize hexokinase-2 (HK2) rather than hexokinase-1 for glycolysis. Accordingly, HK2 inhibitors may selectively target immune cells to suppress post-stroke inflammation. Here we compared the effects of the non-selective hexokinase inhibitor 2-deoxyglucose to the HK2-selective inhibitors lonidamine and 3-bromopyruvate on gene expression changes and secondary injury after stroke.

Methods

Stroke was induced in mouse motor cortex by photothrombosis, and the hexokinase inhibitor

SUBMITTER: Won SJ 

PROVIDER: S-EPMC12570821 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature