Iron overload in CD11c⁺ myeloid cells exacerbates acetaminophen hepatotoxicity.

ABSTRACT: Acute liver injury often progresses to liver failure, with immune responses playing a critical role in regulating the inflammatory process. In this study, we aim to investigate the effects of iron on CD11c⁺ myeloid cells during acetaminophen-induced liver injury. Iron overload caused by F-box and leucine-rich repeat protein 5 (FBXL5) deficiency in CD11c⁺ cells exacerbates liver damage. CD11c⁺ myeloid cell-specific FBXL5-deficient mice exhibit higher serum transaminase levels, liver injury, and mortality than the controls. These phenotypes are associated with enhanced neutrophil infiltration and expression of interleukin (IL)-6, a pro-inflammatory cytokine. Mechanistically, iron overload in FBXL5-deficient cells increases IL-6 production by facilitating the

SUBMITTER: Liu S 

PROVIDER: S-EPMC12540771 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature