Advanced search
Start date
Betweenand

Involvement of NFKB kinase inducer on liver regeneration in mice submitted to partial hepatectomy.

Abstract

In recent decades, obesity and metabolic syndrome have become increasingly prevalent in the world population. Exposure to lipid overload is capable of inducing not only the development of obesity and its complications, such as hepatic steatosis, but also program the individual and its descendants, by epigenetic modifications, to important metabolic changes for several generations. Among the epigenetic mechanisms, microRNAs modulation has gained prominence for its direct action in target genes through post-transcriptional regulation. Consumption of high-fat diet can induce changes in hepatic lipogenesis, oxidative mitochondrial damage and inflammatory processes mediated by changes in the expression of microRNAs, which could increase the predisposition to change as NAFLD, disease characterized by TAG accumulation in hepatocytes, and it takes more than 20% of affected with some type of surgical liver resection. Recent literature suggests that liver fat accumulation can be a detrimental factor in the regenerative process, although the mechanisms involved in this process are not yet well defined. It has been hypothesized that the overactivation of key elements of inflammatory pathways, such as NFkB pathway, can be one of the factors that trigger the failure in the regenerative process, dependent of inflammation. Thus, the objective of this project is to investigate whether obese mice showed worse liver regeneration following surgical resection procedure, resulting from changes in the functioning of non-canonical inflammatory pathway of NFkB and its relationship with the expression of microRNAs involved in the modulation of inflammation, tissue repair and cell cycle. (AU)

Articles published in Agência FAPESP Newsletter about the research grant:
Articles published in other media outlets (0 total):
More itemsLess items
VEICULO: TITULO (DATA)
VEICULO: TITULO (DATA)

Please report errors in scientific publications list by writing to: cdi@fapesp.br.