Introduction |
Dr.Su has been focusing on the field “lipid droplet, lipid droplet proteins, dysregulation of lipid metabolism and metabolic diseases” for a long time with a series work. She purified and established human liver LD-associated proteome and identified an array of proteins differentially expressed in human NALFD. She demonstrated a liver-specific LD protein 17βHSD13 as a pathogenic factor and drug target of NAFLD (2014, 111 (31):11437, PNAS). Since joining Shenzhen University, she carried out several related studies, including: (1) Function study of 17β-HSD13 by using various hsd17b13 (the gene codes 17β-HSD13) genetic edited mice and biochemistry methods; (2) Elucidate the mechanism of lipid dysregulation in acute and chronic liver diseases; (3) Screen of lead compounds that targets 17β-HSD13, FXR, LXR for NAFLD treatment. Dr Su’s original research about 17β-HSD13 provides a potential link between LD proteins and NAFLD, and has been cited by more than 120 papers including papers on NEJM, hepatology, journal of hepatology and so on. She found over-expression of 17β-HSD13 in vivo and in vitro increases size and accumulation of lipid droplets in hepatocytes, which possible mechanism is through enhancement of lipogenesis and maturation of SREBP-1c. Her subsequent work demonstrated 17β-HSD13 was regulated by LXRα agonist T0901317 via a SREBP-1c dependent mechanism (2017, 312(4), Am J Physiol Endocrinol Metab.;2018, 67(supplement 1), Diabetes). She proposed the possible regulation mechanism of 17β-HSD13 and SREBP-1c, and suggested 17β-HSD13 as a potent NASH target (2019, 489:119-125, Mol Cell Enocrinol.). She has 2 patents on 17β-HSD13 and NAFLD drug target. She now successfully constructed 17β-HSD13 liverspecific transgenic, knockout, liver-specific knockout, and two key amino site mutant mice lines, and also a various of HSD17B13 associated plasmid. Her next 5 year-plan include: 1. Define the metabolic phenotypes of those genetically engineered mice; 2. Determine the pathophysiological role of 17βHSD13 during different stages of NAFLD from benign steatosis, NASH to HCC via challenging highfat diet (short term and long term), MCD, and FPC models; 3. Characterize the biological function of 17β-HSD13 by using biochemical, lipidomic, and metabolomic approaches; 4. Study the role 17β-HSD13 in regulating LD generation, growth, fuse, and degradation and the post-translational modification of 17βHSD13. In terms of paper publication and academic effect. Dr.Su’s h-index is 17. |