Recently, a new term, steatotic liver disease (SLD), has been introduced to the field of hepatology to encompass the various etiologies of steatosis. Hepatic steatosis, having an excessive fat accumulation, has been considered a key factor in the progression of serious liver diseases such as hepatic inflammation, fibrosis/cirrhosis, and hepatocellular carcinoma. It could be initiated by an overload of nutrition (e.g., glucose and free fatty acids), intoxicants (e.g., alcohol and endocannabinoid-mediated metabolic dysfunction), or genetic factors. Interestingly, lines of evidence have suggested that beyond its role as a metabolic organ, the liver is considered an immunological and neurological organ due to its diverse metabolic functions, enriched immune cells (e.g., innate and adaptive immune cells), and production and release of hepatotransmitters such as glutamate or 2-arachidonoylglycerol (2-AG).So, these factors might affect the progression of SLD, from simple steatosis to steatohepatitis and fibrosis, by regulating the activation of hepatic stellate cells (HSCs). 

KeyWords: Fibrosis; Hepatic stellate cells; Inflammation; Immunologic factors; Fatty acids