Abstract
There has been a rise in the prevalence of non-alcohol fatty liver disease (NAFLD) due to the popularity of western diets and sedentary lifestyles. One quarter of NAFLD patients is diagnosed with non-alcoholic steatohepatitis (NASH), with histological evidence not only of fat accumulation in hepatocytes but also of liver cell injury and death due to long-term inflammation. Severe NASH patients have increased risks of cirrhosis and liver cancer. In this review, we discuss the pathogenesis and current methods of diagnosis for NASH, and current status of drug development for this life-threatening liver disease.
Highlights
There has been an increased interest in non-alcoholic fatty liver disease (NAFLD), and its advanced stage, non-alcoholic steatohepatitis (NASH) because of their increasing impact on global health [1]
This review focuses on discussing the risks for NASH pathogenesis, current development of biomarkers, and therapeutic target identification for drug development
Galectin-3 protein expression is essential for the development of hepatic fibrosis, which is significantly increased in NASH liver [204]
Summary
There has been an increased interest in non-alcoholic fatty liver disease (NAFLD), and its advanced stage, non-alcoholic steatohepatitis (NASH) because of their increasing impact on global health [1]. In addition to chemokine CCL2, cytokines like TNF-α and IL-1β released from macrophages are important drivers of steatosis, inflammation, and fibrosis in NAFL/NASH [40]. Extensive studies on the gut-liver axis have suggested that intestinal microbiota influenced host susceptibility to obesity, hepatic steatosis, and NASH [142,143,144]. Current progression on developing non-invasive biomarkers is mainly based on the detection of hepatic steatosis [154].
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