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CCL20 is up-regulated in non-alcoholic fatty liver disease fibrosis and is produced by hepatic stellate cells in response to fatty acid loading.

Xin ChuQunyan JinHui ChenG Craig WoodAnthony PetrickWilliam StrodelJon GabrielsenPeter BenottiTooraj MirshahiDavid J CareyChristopher D StillJohanna K DiStefanoGlenn S Gerhard
Published in: Journal of translational medicine (2018)
These results suggest that expression of CCL20, an important inflammatory mediator, is increased in NAFLD fibrosis. CCL20 serves as a chemoattractant molecule for immature dendritic cells, which have been shown to produce many of the inflammatory molecules that mediate liver fibrosis. These data also point to hepatic stellate cells as a key cell type that may respond to lipid loading of the liver.
Keyphrases
  • liver fibrosis
  • induced apoptosis
  • dendritic cells
  • fatty acid
  • cell cycle arrest
  • oxidative stress
  • poor prognosis
  • immune response
  • endoplasmic reticulum stress
  • cell death
  • binding protein
  • deep learning