Neuroblastoma RAS viral oncogene homolog (N-RAS) deficiency aggravates liver injury and fibrosis.

ABSTRACT: Progressive hepatic damage and fibrosis are major features of chronic liver diseases of different etiology, yet the underlying molecular mechanisms remain to be fully defined. N-RAS, a member of the RAS family of small guanine nucleotide-binding proteins also encompassing the highly homologous H-RAS and K-RAS isoforms, was previously reported to modulate cell death and renal fibrosis; however, its role in liver damage and fibrogenesis remains unknown. Here, we approached this question by using N-RAS deficient (N-RAS^-/-) mice and two experimental models of liver injury and fibrosis, namely carbon tetrachloride (CCl₄) intoxication and bile duct ligation (BDL). In wild-type (N-RAS^+/+) mice both hepatotoxic procedures augmented N-RAS expression in the liver. Co

SUBMITTER: Zheng K 

PROVIDER: S-EPMC10415403 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature