| Literature DB >> 28709961 |
Gloria Alvarez-Sola1, Iker Uriarte1, Maria U Latasa2, Maddalen Jimenez2, Marina Barcena-Varela2, Eva Santamaría1, Raquel Urtasun2, Carlos Rodriguez-Ortigosa3, Jesús Prieto3, Pedro Berraondo4, Maite G Fernandez-Barrena3, Carmen Berasain5, Matías A Avila6.
Abstract
The liver has an extraordinary regenerative capacity rapidly triggered upon injury or resection. This response is intrinsically adjusted in its initiation and termination, a property termed the "hepatostat". Several molecules have been involved in liver regeneration, and among them bile acids may play a central role. Intrahepatic levels of bile acids rapidly increase after resection. Through the activation of farnesoid X receptor (FXR), bile acids regulate their hepatic metabolism and also promote hepatocellular proliferation. FXR is also expressed in enterocytes, where bile acids stimulate the expression of fibroblast growth factor 15/19 (FGF15/19), which is released to the portal blood. Through the activation of FGFR4 on hepatocytes FGF15/19 regulates bile acids synthesis and finely tunes liver regeneration as part of the "hepatostat". Here we review the experimental evidences supporting the relevance of the FXR-FGF15/19-FGFR4 axis in liver regeneration and discuss potential therapeutic applications of FGF15/19 in the prevention of liver failure. This article is part of a Special Issue entitled: Cholangiocytes in Health and Disease edited by Jesus Banales, Marco Marzioni, Nicholas LaRusso and Peter Jansen.Entities:
Keywords: Bile acids; Fibroblast growth factor 15/19; Liver regeneration
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Year: 2017 PMID: 28709961 DOI: 10.1016/j.bbadis.2017.06.025
Source DB: PubMed Journal: Biochim Biophys Acta Mol Basis Dis ISSN: 0925-4439 Impact factor: 5.187