Hsa_circ_0001944 Regulates FXR/TLR4 Pathway and Ferroptosis to Alleviate Nickel Oxide Nanoparticles-Induced Collagen Formation in LX-2 Cells.

ABSTRACT: Nickel oxide nanoparticles (NiONPs) can induce liver fibrosis, and their mechanism may be related to non-coding RNA, nuclear receptor signal transduction and ferroptosis, but the regulatory relationship between them is not clear. In this study, we aimed to investigate the role of hsa_circ_0001944 in regulating the Farnesol X receptor (FXR)/Toll-like receptor 4 (TLR4) pathway and ferroptosis in NiONPs-induced collagen deposition. We observed decreased FXR expression, increased TLR4 expression and alterations in ferroptosis features in both the rat liver fibrosis and the LX-2 cell collagen deposition model. To investigate the regulatory relationship among FXR, TLR4 and ferroptosis, we treated LX-2 cells with FXR agonist (GW4064), TLR4 inhibitor (TAK-242) and ferroptosis agonist (Erastin) com

SUBMITTER: Zhou H 

PROVIDER: S-EPMC12031114 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature