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NASH, an advanced form of non-alcoholic fatty liver disease (NAFLD), can progress to liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC)
Genetic factors, environmental factors, and microbiome alterations are mainly involved in disease progression
Experts estimated that 24% of U.S. adults have NAFLD and more than 6.5% of them have NASH (NIH report, 2021). 20~30% of patients with NASH progress to liver fibrosis in 7 years, and 20% of them progress to cirrhosis in two years.
However, since no drugs for NASH are commercially available, off-label drug use is the only available treatment option.
In a mouse model, high-fat diet (HFD) feeding increased both serotonin (5-hydroxytryptamine, 5-HT) levels in the portal blood and serotonin receptor 2a (5-HT receptor 2a, Htr2a) expression in the cell membranes of hepatocytes
Inhibition of gut-derived serotonin synthesis or direct blocking of the 5-HT2a recepto ameliorates hepatic steatosis by suppressing liver Htr2a signaling.
5-HT is also involved in inflammation and fibrosis-related gene expression in the liver and more importantly, the activation of hepatic stellate cells which is directly connected to the progression of liver fibrosis.
The Synthesis of an Htr2a antagonist can provide a potent drug candidate for NASH and liver fibrosis
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