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- W2080881495 abstract "Most cells in mammalian tissues usually contain a diploid complement of chromosomes. However, numerous studies have demonstrated a major role of diploid-polyploid conversion during physiopathological processes in several tissues. In the liver parenchyma, progressive polyploidization of hepatocytes takes place during postnatal growth. Indeed, at the suckling-weaning transition, cytokinesis failure events induce the genesis of binucleated tetraploid liver cells. Insulin signalling, through regulation of the PI3K/Akt signalling pathway, is essential in the establishment of liver tetraploidization by controlling cytoskeletal organisation and consequently mitosis progression. Liver cell polyploidy is generally considered to indicate terminal differentiation and senescence, and both lead to a progressive loss of cell pluripotency associated to a markedly decreased replication capacity. Although adult liver is a quiescent organ, it retains a capacity to proliferate and to modulate its ploidy in response to various stimuli or aggression (partial hepatectomy, metabolic overload (i.e., high copper and iron hepatic levels), oxidative stress, toxic insult, and chronic hepatitis etc.). Here we review the mechanisms and functional consequences of hepatocytes polyploidization during normal and pathological liver growth." @default.
- W2080881495 created "2016-06-24" @default.
- W2080881495 creator A5035622009 @default.
- W2080881495 creator A5064701366 @default.
- W2080881495 creator A5091640131 @default.
- W2080881495 date "2012-01-01" @default.
- W2080881495 modified "2023-10-14" @default.
- W2080881495 title "Hepatocytes Polyploidization and Cell Cycle Control in Liver Physiopathology" @default.
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