Knockdown of SESN2 Exacerbates Cerebral Ischemia-Reperfusion Injury Through Enhancing Glycolysis via the mTOR/HIF-1α Pathway.

ABSTRACT:

Aim

Reprogramming of glycometabolism plays a crucial role in the pathogenesis of cerebral ischemia-reperfusion injury (CIRI). Sestrin2 (SESN2), a sensor upstream of the mTORC1, is closely related to glycometabolism. However, the effect and mechanism of SESN2 in CIRI are unclear. The goal of this research was to explore the effect of SESN2 on CIRI and its potential mechanisms related to glycometabolism.

Methods

Lentiviral vectors carrying SESN2 shRNA (Lenti-SESN2) or negative NC virus (Lenti-GFP) or rapamycin (mTOR inhibitor) were employed in the oxygen-glucose deprivation/reoxygenation (OGD/R) model and in the middle cerebral artery occlusion (MCAO) mice. In all, 3 days after I/R, neurological deficit scores and infarct size were assessed. The glycolysis and SESN2 levels wer

SUBMITTER: Wang Z 

PROVIDER: S-EPMC11875773 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature