TRIM16 mediates YAP1 K63-linked ubiquitination to alleviate sepsis-induced acute liver injury through YAP/Nrf2 axis in mice.

ABSTRACT: Sepsis-induced liver injury is associated with high morbidity and mortality, yet its underlying mechanisms remain elucidated. In this study, we observed a significant reduction in the E3 ubiquitin ligase TRIM16 in lipopolysaccharide (LPS)-injured hepatocytes; however, its functional role and regulatory mechanisms were unclear. Using in vitro LPS-induced hepatocyte injury and in vivo cecal ligation and puncture (CLP)-induced septic liver injury models, we investigated TRIM16's effects via small interfering RNA and AAV9-overexpression plasmids in hepatocytes. Results demonstrated that TRIM16 overexpression rescued LPS-induced suppression of hepatocyte viability, reduced cellular dysfunction (ALT, AST), and significantly suppressed pro-inflammatory cytokine expression (TNF-α, IL-6) and oxidat

SUBMITTER: Zhang K 

PROVIDER: S-EPMC12838455 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature