Udayan M. Apte, Ph.D. DABT
Dr. Apte is a toxicologist and a liver pathobiologists. His research is focused on mechanisms of liver regeneration, drug-induced liver injury, pathogenesis of liver cancer and effects of perfluorinated chemicals on the liver. Dr. Apte teaches toxicology to graduate students and medical students, and serves as a course director for two main toxicology courses in his department.
Dr. Apte is also a board certified toxicologist and is a member of the US EPA's Scientific Advisory Committee on Chemicals (SACC).
Education and Training
- BSc, Zoology, Willingdon College, Sangli, India
- MSC, Cell Biology, Shivaji University, Kolhapur, India
- PhD, Toxicology, The University of Louisiana at Monroe, Monroe, LA, USA
- Post Doctoral Fellowship, Alcoholic Liver Disease, Texas A&M University, College Station, TX
- Post Doctoral Fellowship, Liver regeneration and pathogenesis of liver cancer, University of Pittsburgh School of Medicine, Pittsburgh, PA
Licensure, Accreditations & Certifications
- Diplomate, American Board of Toxicology
Dr. Apte leads an NIH-funded research program focused on determining the mechanisms liver differentiation, liver regeneration, liver cancer and the adverse effect of environmental contaminants on the liver. There are three main and inter-linked areas of research in the laboratory. First, we have been investigating the mechanisms of liver regeneration and recovery after acetaminophen (APAP) overdose, which is the most common cause of acute liver failure in the Western world. Mechanisms of APAP-induced liver injury have been investigated for decades but the mechanisms of liver regeneration and recovery are relatively less studied, despite significant therapeutic potential. Secondly, we are studying mechanisms that balance hepatocyte differentiation and hepatocyte proliferation. In this project, we are studying the role of a nuclear receptor called HNF4a, which is a master regulator of hepatic differentiation and a major tumor suppressor in the liver. Finally, we are investigating the mechanisms of liver injury induced by persistent organic chemicals called poly and perfluorinated chemicals. We use complex tissue and cell specific knockout and transgenic mouse models combined with Next Generation Sequencing technology in our research.
- Bhushan, B, Walesky, C, Manley, M, Gallagher, T, Borude, P, Edwards, G, Monga, S., P, Apte, U. 2014. Pro-regenerative signaling after acetaminophen-induced acute liver injury in mice identified using a novel incremental dose model.. The American journal of pathology, 184 (11), 3013-25
- Walesky, C, Edwards, G, Borude, P, Gunewardena, S, O'Neil, M, Yoo, B, Apte, U. 2013. Hepatocyte nuclear factor 4 alpha deletion promotes diethylnitrosamine-induced hepatocellular carcinoma in rodents.. Hepatology (Baltimore, Md.), 57 (6), 2480-90
- Huck, I, Gunewardena, S, Espanol-Suner, R, Willenbring, H, Apte, U. 2018. Hepatocyte Nuclear Factor 4 alpha (HNF4α) Activation is Essential for Termination of Liver Regeneration.. Hepatology (Baltimore, Md.)
- Beggs, K., M, McGreal, S., R, McCarthy, A, Gunewardena, S, Lampe, J., N, Lau, C, Apte, U. 2016. The role of hepatocyte nuclear factor 4-alpha in perfluorooctanoic acid- and perfluorooctanesulfonic acid-induced hepatocellular dysfunction.. Toxicology and applied pharmacology, 304, 18-29
- Poudel, Samikshya, Cabrera, Diego., Paine, Bhushan, Bharat, Manley Jr, Michael, Gunewardena, Sumedha, Jaeschke, Hartmut, Apte, Udayan. 2021. Hepatocyte-Specific Deletion of Yes-Associated Protein Improves Recovery From Acetaminophen-Induced Acute Liver Injury. Toxicological Sciences, 184 (2), 276-285.