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. 2022 Aug 23;65:101581. doi: 10.1016/j.molmet.2022.101581

Figure 2.

Figure 2

miR-34a in NAFLD/NASH. Expression of miR-34a was shown to increase with NAFLD progression and to be controlled through pathways involving FXR, PU.1, JNK1, LXRα and IRE1α. Altered expression/activities of these upstream regulators in NAFLD might contribute to the elevated levels of miR-34a with disease progression. Several miR-34a targets were identified in NAFLD, including SIRT1, HNF4α, PPARα, ATG4B and RAB8B in hepatic lipid metabolic pathways (repressing fatty acid (FA) oxidation and inducing lipogenesis and cholesterol synthesis), p66Shc to stimulate hepatocyte apoptosis, and SIRT1 and PPARγ to stimulate hepatic stellate cell (HSC) activation and fibrosis. Grey arrows: Regulation of upstream factors found to control miR-34a expression in NAFLD/NASH. Red arrows: Increased or decreased activities in pathways/processes as a result of miR-34a actions, leading to unfavourable effects on liver metabolic function and progression of NAFLD.