Figure 1.

The gut-liver axis: MAFLD induces profound alterations in the gut-liver axis. Beneficial autochthonous bacteria are replaced by potentially pathogenic species leading to dysbiosis and bacterial overgrowth. The increased penetrability of the mucus layer and the increased permeability of the epithelial and vascular barriers allow the translocation of bacteria and related products. Bacterial translocation promotes the activation of gut and liver pro-inflammatory pathways, which play a key role in the pathogenesis of MAFLD. SCFAs: short-chain fatty acids; FXR: Farnesoid X receptor; TLR: toll-like receptor.