miR-22 inhibition reduces hepatic steatosis via FGF21 and FGFR1 induction.

ABSTRACT:

Background & aims

Metabolism supports cell proliferation and growth. Surprisingly, the tumor suppressor miR-22 is induced by metabolic stimulators like bile acids. Thus, this study examines whether miR-22 could be a metabolic silencer.

Methods

The relationship between miR-22 and the expression of fibroblast growth factor 21 (FGF21) and its receptor FGFR1 was studied in cells and fatty livers obtained from patients and mouse models. We evaluated the effect of an miR-22 inhibitor alone and in combination with obeticholic acid (OCA) for the treatment of steatosis.

Results

The levels of miR-22 were inversely correlated with those of FGF21, FGFR1, and PGC1α in human and mouse fatty livers, suggesting that hepatic m

SUBMITTER: Hu Y 

PROVIDER: S-EPMC7078383 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature