Activation of the Nrf2/HO-1 axis by glutaredoxin 2 overexpression antagonizes vascular endothelial cell oxidative injury and inflammation under LPS exposure.

ABSTRACT: Atherosclerosis constitutes a proverbial pathogenic mechanism for cardio-cerebrovascular disease that accounts for the most common cause of disability and morbidity for human health worldwide. Endothelial dysfunction and inflammation are the key contributors to the progression of atherosclerosis. Glutaredoxin 2 (GLRX2) is abundantly existed in various tissues and possesses a range of pleiotropic efficacy including anti-oxidative and anti-inflammatory responses. However, its role in atherosclerosis is still undefined. Here, down-regulation of GLRX2 was validated in lipopolysaccha (LPS)-induced vascular endothelial cells (HUVECs). Moreover, elevation of GLRX2 reversed the inhibition of cell viability in LPS-treated HUVECs and decreased LPS-induced increases in cell apoptosis and caspase-3 ac

SUBMITTER: Liu Y 

PROVIDER: S-EPMC10940561 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature