Abstract
Non-alcoholic fatty liver disease (NAFLD) is emerging as one of the most common chronic liver diseases in developed western countries. Non-alcoholic steatohepatitis (NASH) is the most severe form of NAFLD, and can progress to more severe forms of liver disease, including fibrosis, cirrhosis, and even hepatocellular carcinoma. The activation of hepatic stellate cells plays a critical role in NASH-related fibrogenesis. Multiple factors, such as insulin resistance, oxidative stress, pro-inflammatory cytokines and adipokines, and innate immune responses, are known to contribute to the development of NASH-related fibrogenesis. Furthermore, these factors may share synergistic interactions, which could contribute to the process of liver fibrosis. Given the complex etiology of NASH, combined treatment regimes that target these different factors provide potential treatment strategies for NASH-related liver fibrosis.
Highlights
Non-alcoholic fatty liver disease (NAFLD), affects one-third of adults and an increasing percentage of children in developed countries (Cohen et al, 2011)
It is well-known that the activation of hepatic stellate cells (HSCs) is one of the critical events in non-alcoholic steatohepatitis (NASH)-related fibrogenesis
Oxidative stress, pro-inflammatory cytokines, adipokines, and the innate immune response are involved in the phenotypic transition of HSCs (Figure 1), which results in the development of NASH-related hepatic fibrogenesis
Summary
Non-alcoholic fatty liver disease (NAFLD), affects one-third of adults and an increasing percentage of children in developed countries (Cohen et al, 2011). The disease spectrum of NAFLD includes simple steatosis, which is relatively benign, non-alcoholic steatohepatitis (NASH), NASH-related hepatic fibrosis, and cirrhosis (Jou et al, 2008). Characterizing the mechanisms of hepatic fibrogenesis in NASH is critical for preventing disease progression and improving the prognosis of patients with NAFLD. Understanding NASH-related hepatic fibrogenesis is an important research area and will be valuable for identifying potential therapeutic targets to prevent the progression of NAFLD to NASH and more severe disease. ACTIVATION OF HEPATIC STELLATE CELLS Hepatic fibrosis, which is characterized by the excessive deposition of extracellular matrix (ECM) proteins, is considered to be a wound-healing process that results from a variety of chronic stimuli (Tsukada et al, 2006), such as viral hepatitis, NASH, or alcoholic liver disease. The role of HSC activation in NAFLD has not been clarified completely, several studies have reported increased HSC activation in NASH (Kaji et al, 2011)
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