Fig. 5
From: Targeting protein modifications in metabolic diseases: molecular mechanisms and targeted therapies
Overview of the roles of PTM in fatty liver diseases. Non-alcoholic fatty liver disease (NAFLD) is characterized by fat accumulation in the liver. We summarize the diverse roles of PTMs in the pathogenesis of NAFLD to enrich the understanding of the molecular mechanisms of the intricate interrelationship between post-translational modification (PTM) of important factors and fatty liver disease. (1) Multiple endogenous and exogenous stimuli can lead to aberrant dynamic proteins posttranslational modifications to result in chronic liver disease. (2) Many proteins have multiple modification sites to modulate lipid synthesis, lipolysis, and fatty acid oxidation by phosphorylation, acetylation or SUMOylation of key substrates, such as ACC, SREBPs, GPAT and FXR. Activation and inhibition effects are displayed in “arrows” and “inhibitors”, respectively. The figure is generated with BioRender (https://biorender.com). AKT protein kinase B, ACLY ATP citrate lyase, ACC acetyl CoA carboxylase, ChREBP carbohydrate response element binding protein, FFAs free fatty acids, FASN fatty acid synthase, FXR farnesoid X receptor, FGF19 fibroblast growth factor 19, FATP fatty acid transport protein, GSK-3 glycogen synthase kinase 3, JNK c-Jun N-terminal kinase, MEKK mitogen-activated extracellular signal-regulated kinase kinase, Nck non-catalytic region of tyrosine kinase adaptor protein, NEFA non-esterified fatty acids, PAK p21-activated kinase, SREBP1 sterol-regulatory element binding protein 1, STAT5 signal transducer and activator of transcription 5, SCD1 stearoyl-CoA desaturase 1, TRAF TNF receptor associated factors
