Placental growth factor modulates endothelial NO production and exacerbates experimental hepatopulmonary syndrome.

ABSTRACT:

Background & aims

Hepatopulmonary syndrome (HPS) results from portal hypertension, with or without cirrhosis, and is marked by pulmonary vascular dilations leading to severe hypoxemia. Although placental growth factor (PlGF) is important for vascular growth and endothelial function, its role in HPS is unclear. This study investigated the involvement of PlGF in experimental models of HPS and in patients.

Methods

Circulating PlGF levels were measured in 64 controls and 137 patients with liver disease, with or without HPS. Two rat models, common bile duct ligation (CBDL) and long-term partial portal vein ligation (PPVL), were used. Plgf-knockout (Plgf ^-/-) rats were generated using CRISPR-Cas9. Lung RNA-sequencing analysis was performed in the CB

SUBMITTER: Robert F 

PROVIDER: S-EPMC11840504 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature