Assistant Professor

• Gastroenterology and Nutrition
• Developmental Biology and Genetics
• David A. Rudnick Research Lab

Dr. David Rudnick went to University of Illinois and then completed M.D. and Ph.D. studies at Washington University School of Medicine. His Ph.D. thesis, done in Dr. Jeffrey Gordon's lab, focused on understanding the enzymatic reaction mechanism and substrate specificity of protein-N-myristoylation. He received the Morris Alex Prize, the Needleman Pharmacology Award and the George F. Gill Prize in Pediatrics during his medical school education. He finished a residency in Pediatrics at St. Louis Children's Hospital. After his clinical training in Pediatric Gastroenterology and Nutrition, he began working with Drs. David Perlmutter and Louis Muglia on investigating the molecular mechanisms of liver regeneration in animal models of pediatric liver diseases. He joined the staff of our division with an NIH KO8 Award and an AGA Research Scholar Award. His lab focuses on studying mechanisms of liver regeneration.

Dr. Rudnick has shown that prostaglandins, specifically those derived from COX-2, are required for the initiation of liver regeneration, and function via a signaling pathway that appears to be distinct from the TNFa /IL-6/STAT3-dependent pathway. The lab uses knockout mice in the partial hepatectomy model system as well as state-of-the-art functional genomics and proteomics to further examine the initiation of liver regeneration as well as to begin to define the signals involved in the precise termination of liver regeneration after restoration of the appropriate liver to body weight ratio. Lessons learned about liver regeneration in the murine hepatectomy model system are being applied to other models of hepatocyte proliferation, including animal models of metabolic liver disease and hepatocyte transplantation, to begin to dissect the similarities and differences in the signaling pathways that regulate the proliferative response in these different settings. Clinical experience suggests that it is derangement of the hepatic regenerative response in the setting of chronic liver injury that can lead to cirrhosis or hepatocellular carcinoma. Understanding the signal transduction pathways that modulate the hepatic regenerative response in greater detail may ultimately lead to the design of novel therapeutic interventions to prevent or even reverse these outcomes.