1. Introduction
skeletal muscle, hepatocellular lipid, inflammation, fibrosis, NASH, fibrogenesis, Non-Alcoholic Steatohepatitis, steatosis, liver cell injury
INFLAMMATION, LIVER DAMAGE, FIBROSIS, LIVER FIBROSIS, INSULIN RESISTANCE, PATHOGENESIS, STEATOSIS, CHRONIC LIVER DISEASE
Non-Alcoholic Steatohepatitis (NASH) is a potentially fatal chronic liver disease. NASH is an emerging public health issue, characterized by inflammation, hepatocellular lipid buildup, liver cell injury in the form of hepatocyte ballooning, and steatosis both with or without fibrosis in lack of excessive alcohol intake [Despite continuous progress in understanding the pathogenesis of NASH, finding potential therapeutic targets, and progressing drug development, there are substantial unresolved challenges, and there is presently no FDA-approved drug for NASH [Peroxisome Proliferator activated receptor (PPARs), a therapeutic target that functions as a master regulator in the liver and adipose tissue has gained prominence over recent years. The deregulation of PPAR accelerates the progression of NASH by influencing inflammation, lipid metabolism, insulin resistance, and fibrogenesis. PPARs are activated by ligands and bind to fatty acids. It belongs to the Nuclear Hormone receptors superfamily which play an essential role in whole-body energy metabolism [PPARα expresses in the adipose tissue, liver, kidney, heart, and skeletal muscle [Previous studies have demonstrated that activating one or more PPAR isoforms has therapeutic benefits in preclinical models of liver damage. PPAR activation has been shown to cure moderate liver fibrosis, decrease steatosis, inflammation and alleviate the extrahepatic consequences of chronic liver disease [