Chloroquine Restores eNOS Signaling in Shunt Endothelial Cells via Inhibiting eNOS Uncoupling.

ABSTRACT: Pulmonary arterial hypertension (PAH) is characterized by increased lung vascular stiffness and impaired vessel relaxation, primarily due to reduced nitric oxide (NO) production in endothelial cells. Recent studies indicate that chloroquine, an autophagy inhibitor, may help lower pulmonary arterial pressure and enhance lung vascular function. This study investigates the mechanisms underlying the chloroquine-mediated restoration of NO bioavailability in endothelial cells derived from aortopulmonary shunt lambs, a relevant model for congenital heart defect (CHD)-associated PAH. We found that NO production was significantly reduced in shunt pulmonary artery endothelial cells (PAECs), attributable to decreased levels of tetrahydrobiopterin (BH₄) and diminished expression of GTP cycl

SUBMITTER: Liang Y 

PROVIDER: S-EPMC11818845 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature