Endogenous C-type natriuretic peptide offsets the pathogenesis of steatohepatitis, hepatic fibrosis, and portal hypertension.

ABSTRACT: Metabolic dysfunction-associated steatotic liver disease (MASLD), hepatic fibrosis, and portal hypertension constitute an increasing public health problem due to the growing prevalence of obesity and diabetes. C-type natriuretic peptide (CNP) is an endogenous regulator of cardiovascular homeostasis, immune cell reactivity, and fibrotic disease. Thus, we investigated a role for CNP in the pathogenesis of MASLD. Wild-type (WT), global CNP (gbCNP^-/-), and natriuretic peptide receptor-C (NPR-C^-/-) knockout mice were fed a choline-deficient defined amino acid diet or administered CCl₄. Liver damage was assessed by histological and biochemical analyses, with steatosis and portal vein size determined by ultrasound. Portal vein pressure and reactivity were measured

SUBMITTER: Perez-Ternero C 

PROVIDER: S-EPMC11734523 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature