Fig. 2

Showing that the increased expression of certain genes and proteins related to inflammatory, fats, and extracellular matrix (ECM) pathways in early stage of NAFLD to liver-fibrosis stage. The early stage of the disease started from the small amount of fat deposition in liver parenchyma, but progressively, mode of liver disease converted into non-alcoholic steatohepatitis with inflammatory signatures shows increased expression of interlekin-6 (IL-6), interleukin-8 (IL-8), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), Toll-like receptor-4 (TLR-4), C-reactive protein (CRP), and nuclear factor-kappa beta (NF-kappa β). Activation of fat-related pathways like fatty acid-binding protein-4 (FABP4) and cluster of differentiation 36 (CD36). At the stage of NASH, the lipid droplet-associated proteins perilipin-1 (PLIN1) is highly expressed. Some other NASH-related proteins expression like cytokeratin 18 (CK18), cathepsin D, and ferritin. At this stage, some studies indicate that the disease can be reverse using the combine therapy of vitamin E, pioglitazone, and liraglutide. But after crossing the NASH stage, the liver entered into the emergency zone; the stage is known as liver fibrosis or cirrhosis condition where only liver transplantation is the single option to save the life of the patient. The fibrosis stage begins with increased expression of extracellular matrix proteins like hyaluronic acid, laminin, tissue inhibitor of metalloproteinase (TIMP-1), ferritin, alanine transaminase (ALT), aspartate transaminase (AST), procollagen peptide type III (PIIINP), matrix metalloproteinase (MMP), and procollagen C3 (Pro C3)