Non-alcoholic fatty liver disease (NAFLD) is emerging as one of the most common chronic liver sicknesses in developed western countries. Non-alcoholic steatohepatitis (NASH) is the most extreme form of NAFLD, and may develop into more severe types of liver disease, consisting of fibrosis, cirrhosis, or even hepatocellular carcinoma. The activation of hepatic stellate cells performs a critical role in NASH-related fibrogenesis. Multiple factors, together with insulin resistance, oxidative strain, pro-inflammatory cytokines and adipokines, and innate immune responses, are acknowledged to make a contribution to the development of NASH-related liver fibrogenesis. Furthermore, those elements may share synergistic interactions, that could make a contribution to the process of liver fibrosis. Given the complex etiology of NASH, combined treatment regimes that target those different factors offer potential treatment strategies for NASH-associated liver fibrosis.

Hepatic fibrosis, which is characterized by the excessive deposition of extracellular matrix (ECM) proteins, is taken into consideration to be a wound-healing process that effects by a variety of chronic stimuli, together with viral hepatitis, NASH, or alcoholic liver disease. In-person NASH-associated fibrosis, ECM is deposited frequently in the zone 3 perisinusoidal areas of Disse, after which spreads to surround hepatocytes and thicken the distance of Disse; forming feature “chicken-wire” fibrosis. Eventually, the pericentral fibrosis forms septa to isolate regenerating nodules.

NASH presently represents one of the most prevalent liver diseases in humans, that is secondary to the increasing prevalence of obesity and metabolic syndrome. It is famous that the activation of HSCs is one of the critical events in NASH-associated liver fibrogenesis. Insulin resistance, oxidative stress, pro-inflammatory cytokines, adipokines, and the innate immune reaction are concerned with involved in the phenotypic transition of HSCs, which then affects withinside the improvement of NASH-associated hepatic fibrogenesis. Of course, there are different elements we now no longer noted here, together with endocannabinoid system and renin-angiotensin-aldosterone system. Because they may be not as feature as insulin resistance and oxidative stress in NASH, even though they play roles in NASH- associated fibrogenesis. All those elements can also additionally have interaction with every other and form a unique network that ends in the pathogenesis of liver fibrosis. Combined remedies focused to those various factors are a viable strategy in NASH-associated liver fibrosis. In addition, an ideal animal model of NASH will assist us to characterize the mechanisms of liver fibrosis in metabolic syndrome and to identify novel therapeutic approaches in the treatment of liver fibrosis.