Inhibition of p66Shc Oxidative Signaling via CA-Induced Upregulation of miR-203a-3p Alleviates Liver Fibrosis Progression.

ABSTRACT: We previously found that inhibition of p66Shc confers protection against hepatic stellate cell (HSC) activation during liver fibrosis. However, the effect of p66Shc on HSC proliferation, as well as the mechanism by which p66Shc is modulated, remains unknown. Here, we elucidated the effect of p66Shc on HSC proliferation and evaluated microRNA (miRNA)-p66Shc-mediated reactive oxidative species (ROS) generation in liver fibrosis. An in vivo model of carbon tetrachloride (CCl₄)-induced liver fibrosis in rats and an LX-2 cell model were developed. p66Shc expression was significantly upregulated in rats with CCl₄-induced liver fibrosis and in human fibrotic livers. Additionally, p66Shc knockdown in vitro attenuated mitochondrial ROS generation and HSC proliferation. Interes

SUBMITTER: Wang Z 

PROVIDER: S-EPMC7417942 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature