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• W3136542014 abstract "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.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-fibrotic patients.In TAA-induced fibrotic mice, ALPPS-induced regeneration was significantly inferior to that of the control group (P=0.027 at day 2 and P<0.001 at day 7). Furthermore, mitochondria-associated genes were significantly downregulated in TAA-challenged mice. Accordingly, the reduced production of ATP and elevated levels of malondialdehyde indicated disturbances in intracellular energy metabolism during the ALPPS-induced regenerative process after TAA treatment. Further investigations were performed in TGF-β1-treated AML12 cells and CCl4-treated mice, which indicated that mitochondrial dysfunction attenuated the capacity for rapid regeneration after ALPPS.In summary, this study revealed that mitochondrial dysfunction led to inferior regeneration in livers with toxin-induced fibrosis and identified new therapeutic targets to improve the feasibility and safety of the ALPPS procedure. Further studies in human patients are required in the future." @default.
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• W3136542014 date "2021-04-01" @default.
• W3136542014 modified "2023-09-23" @default.
• W3136542014 title "Mitochondrial dysfunction attenuates rapid regeneration in livers with toxin-induced fibrosis" @default.
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• W3136542014 doi "https://doi.org/10.21037/atm-20-4639" @default.
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