Metabolic Associated Fatty Liver Disease (MAFLD) is a metabolic disorder which is affected by multiple factors, such as genetic and environmental influences. It can lead to elevated risks of cirrhosis and liver cancer as well as a higher incidence of atherosclerotic cardiovascular and cerebrovascular diseases, chronic kidney disease, and tumors. Insulin resistance, endoplasmic reticulum stress, intestinal flora disturbance, and genetic factors may be involved in the progression of MAFLD, but the pathogenesis has not been fully elucidated.
On March 14, 2023, the research team of Professor Huang Ailong and Tang Ni from CQMU’s Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education) released their latest findings online, titled “Deficiency of gluconeogenic enzyme PCK1 promotes metabolic-associated fatty liver disease (MAFLD) through PI3K/AKT/PDGF axis activation in male mice”. For the first time, this study revealed that the deletion of phosphoenolpyruvatecarboxy kinase 1 (PCK1) triggered lipid deposition in hepatocytes, which in turn activated stellate cells through activated RhoA/PI3K/AKT/PDGF-AA signaling axis and thus inducing liver fibrosis. Targeting the RhoA/AKT signaling pathways and other intervention strategies could potentially offer novel therapeutic approaches and targets for MAFLD.
