Researchers have found that a gene known as AEBP1 may play a central role in the development, severity, and potential treatment of liver disease, according to a study by Temple University, the Geisinger Obesity Institute, and the Translational Genomics Research Institute (TGen), an affiliate of City of Hope. The findings are detailed in a study published online on July 12, 2019 in PLoS One. The open-access article is titled “AEBP1 Expression Increases with Severity of Fibrosis in NASH and Is Regulated by Glucose, Palmitate, and miR-372-3p.” The study results suggest that increased expression of AEBP1 correlates with the severity of liver fibrosis in patients with NASH (nonalcoholic steatohepatitis), which is a type of NAFLD (nonalcoholic fatty liver disease), the most common cause of liver damage. NASH indicates there is both inflammation and liver cell damage, along with fat in the liver. "Given the strong link between fibrosis and risk of liver-related mortality, efforts to identify and characterize the specific mechanisms contributing to NAFLD progression are critical for the development of effective therapeutic and preventative strategies," said Dr. Johanna DiStefano, Head of the Diabetes and Fibrotic Disease Unit at TGen and senior author of the PLoS article. One of the study's major findings is that AEBP1 regulates the expression of a network of at least nine genes related to fibrosis: AKR1B10, CCDC80, DPT, EFEMP1, ITGBL1, LAMC3, MOXD1, SPP1, and STMN2. "These findings indicate that AEBP1 may be a central regulator of a complex fibrosis gene expression network in the human liver," said Dr. DiStefano.
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