Iron chelation as a new therapeutic approach to prevent senescence and liver fibrosis progression.

ABSTRACT: Iron overload and cellular senescence have been implicated in liver fibrosis, but their possible mechanistic connection has not been explored. To address this, we have delved into the role of iron and senescence in an experimental model of chronic liver injury, analyzing whether an iron chelator would prevent liver fibrosis by decreasing hepatocyte senescence. The model of carbon tetrachloride (CCl₄) in mice was used as an experimental model of liver fibrosis. Results demonstrated that during the progression of liver fibrosis, accumulation of iron occurs, concomitant with the appearance of fibrotic areas and cells undergoing senescence. Isolated parenchymal hepatocytes from CCl₄-treated mice present a gene transcriptomic signature compatible with iron accumulation and

SUBMITTER: Amengual J 

PROVIDER: S-EPMC11408630 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature