Mitochondrial dysfunction attenuates rapid regeneration in livers with toxin-induced fibrosis.

ABSTRACT:

Background

The mechanism of associating liver partition and portal vein ligation for staged hepatectomy (ALPPS)-induced rapid liver regeneration remains poorly documented, especially in patients with fibrosis. Therefore, this study aims to investigate the underlying mechanism of ALPPS-induced accelerated regeneration in toxin-induced fibrosis models.

Methods

The ALPPS-induced regeneration model was established in livers with thioacetamide (TAA)-induced fibrosis to determine the regenerative pathways involved in rapid regeneration. Confirmatory experiments were performed in transforming growth factor beta 1 (TGFβ1)-treated AML12 cells and mice with carbon tetrachloride (CCl₄)-induced fibrosis. Finally, mitochondrial dysfunction was validated in fibrotic/non-fibroti

SUBMITTER: Li Z 

PROVIDER: S-EPMC8105818 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature