Liver sphingomyelin synthase 1 deficiency causes steatosis, steatohepatitis, fibrosis, and tumorigenesis: An effect of glucosylceramide accumulation
Zhiqiang Li, Yeun-po Chiang, Mulin He, Tilla S. Worgall, Hongwen Zhou, Xian‐Cheng Jiang
Abstract
) promoted hepatocyte to secrete more activated TGFβ1, which stimulated more collagen 1α1 production in hepatic stellate cells. Additionally, GluCer promoted more β-catenin translocation into the nucleus, thus promoting tumorigenesis. Importantly, human NASH patients had higher liver GluCer synthase and higher plasma GluCer. These findings implicated that GluCer accumulation is one of triggers promoting the development of NAFLD into NASH, then, fibrosis, and tumorigenesis.
Topics & Concepts
SteatosisLipogenesisSteatohepatitisInternal medicineEndocrinologyCarcinogenesisFibrosisSphingomyelinInflammationBiologyHepatocyteChemistryCancer researchFatty liverLipid metabolismBiochemistryMedicineCancerIn vitroCholesterolDiseaseSphingolipid Metabolism and SignalingLiver physiology and pathologyLipid metabolism and biosynthesis