The overarching goal of Natasha Snider’s research is to promote discovery of pharmacological agents to halt the progression of chronic liver diseases. She has investigated various aspects of liver function: toxicity mechanisms (as an undergraduate student), pharmacology and drug metabolism (as a graduate student), and disease pathogenesis (as a postdoctoral fellow). During her postdoctoral training at the University of Michigan, she identified sex- and genetic background- associated susceptibility factors for liver injury. She identified ecto-5’-nucleotidase (CD73) as a critical regulator of Mallory-Denk body – associated hepatocyte injury and discovered a novel human-specific isoform (CD73S) produced by alternative splicing in cirrhotic, but not normal livers. The goal of her current R01 grant is to define the precise functional mechanisms of CD73 in hepatocyte injury and liver disease. She was awarded the American Physiological Society 2019 New Investigator Award.
Relevance of Research to CGIBD Mission: The target of Natasha Snider’s research is the progression of chronic liver diseases.
CGIBD Focus Area(s): Regenerative Medicine/Repair
Pilot Feasibility Award 2016