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

Figure 4.

Figure 4

miR-21 in NAFLD/NASH. Expression levels of miR-21 were found to increase with NAFLD progression. miR-21 expression is controlled through pathways involving STAT3, NF-κB and AP-1. Some studies demonstrate a role of miR-21 in early NAFLD pathogenesis, where PPARα is a direct miR-21 target, while other studies suggest that miR-21 is involved in later NAFLD stages only. miR-21 was shown to decrease hepatic insulin sensitivity and gluconeogenesis and to promote steatosis. miR-21 has also been implicated in NAFLD progression to NASH by inducing fibrosis via hepatic stellate cell (HSC) activation and epithelial–mesenchymal transition (EMT) of hepatocytes by repression of SPRY2, HNF4α, PTEN, LRP6 and SMAD7. Some studies point to a central role of miR-21 in aggravating hepatocyte injury as well as liver inflammation and fibrosis, while other studies suggest that miR-21 might be dispensable for these processes. Grey arrows: Regulation of upstream factors found to control miR-21 expression in NAFLD/NASH. Red arrows: Increased or decreased activities in pathways/processes as a result of miR-21 actions, leading to unfavourable effects on liver metabolic function and progression of NAFLD.