Satdarshan (Paul) Singh Monga, MD
Professor of Pathology
Professor in Experimental Pathology


Dr. Monga is the Chair for Experimental Pathology, Vice Chair and Chief of Division of Experimental Pathology, Professor of Pathology (Division of Experimental Pathology), Professor of Medicine (Division of Gastroenterology, Hepatology & Nutrition), Assistant Dean for Medical Scientist Training Program, Director of Cellular Approaches to Tissue Engineering & Regeneration (CATER) Program, Associate Director of the University of Pittsburgh Drug Discovery Institute (UPDDI), and Director of the Pittsburgh Liver Research Center.

Office Location:
S-422 BST
200 Lothrop Street
Pittsburgh PA 15261
Contact Information:
Office Telephone: 412-648-8842
Email: smonga@pitt.edu
or mongass@upmc.edu

Education

  • MD - Dayanand Medical College & Hospital, Ludhiana, India, 1993
  • Postdoctoral Fellowship - Georgetown University, 1997
  • Postdoctoral Fellowship - Temple University, 1999

Research Expertise

For around 21 years, my research has focused on understanding the cellular and molecular basis of liver health and disease. Specifically, my lab has a longstanding interest in understanding the role of cellular and molecular signaling in liver development, regeneration, inflammation, injury, fibrosis and tumorigenesis. Being in the field for around 20 years, we have generated many novel and innovative tools to study liver. Using GEMM models, AAV systems, lipid nanoparticles, imaging modalities and others, we have been able to identify role of pathways such as Wnt, Yap and others in both hepatic physiology and pathology. The eventual goal of the lab is to gain better understanding of molecular aberrations for improved therapeutics for various hepatic diseases such as end stage liver disease (ESLD), liver failure, injury, fibrosis and cancer. The eventual goal of the lab is to gain better understanding of molecular aberrations in various hepatic diseases for improved clinical outcomes. One major focus of the lab is to understand subsets of human HCC through better and more representative disease modeling. The starting point of the investigation is human HCC analysis to identify novel combinatorial aberrations in the form of mutations and/or expression changes in specific genes. Such combinations are then expressed through innovative technology in a subset of hepatocytes in mice. Appearance of HCC supports the oncogenic nature of the co-occurrences and concordance between gene expression from human HCC subset with such co-occurrences and HCC in mice generated through expression of these co-occurrences supports validity of the model in recapitulating human disease. We then use such models to study HCC pathogenesis in that subset to address tumor biology, progression and therapeutics for translation into patients. This is an interesting approach from bedside to bench and back. Because of liver's regenerative potential, there are innovative opportunities to develop therapies for ESLD. Ongoing research is focusing on innovations in surgery, stem cell biology, cellular reprogramming, cell therapy, and hepatic tissue engineering, broadly categorized under the Hepatic Regenerative Medicine. Our lab has focused on elucidating role and regulation of complex cell-molecule circuitry of the highly relevant pathways such as Wnt/ ?-catenin in liver physiology especially in metabolic zonation and regeneration, which we believe will be prudent for the continued success of hepatic regenerative medicine as a discipline and expected to yield better therapies for patients with chronic liver disease, cirrhosis and ESLD.

NIH Research

View Dr. Monga's NIH RePORT on nih.gov

Selected Publications

View Dr. Monga's publications on PubMed

  • Pradhan-Sundd T, Liu S, Singh S, Podder M, Ko S, Bell A, Franks J, Huck I, Stolz D, Apte U, Ranganathan S, Nejak-Bowen K, Monga SP. Dual β-catenin and β-catenin loss in hepatocytes impacts their polarity through altered transforming growth factor beta and hepatocyte nuclear factor 4 alpha signaling. Am J Pathol. 2021 Mar 1:S0002 9440(21)00075-4. doi:10.1016/j.ajpath.2021.02.008. Epub ahead of print. PMID: 33662348.
  • Tao J, Krutsenko Y, Moghe A, Singh S, Poddar M, Bell A, Oertel M, Singhi A, Geller DA, Chen X, Lujambio A, Liu S, Monga SP. Nrf2 and β -catenin activation in hepatocellular cancer: Biological and Therapeutic Implications. Hepatology. 2021 Feb 2. doi: 10.1002/hep.31730. Epub ahead of print. PMID: 33529367.
  • Adebayo Michael AO, Ko S, Tao J, Moghe A, Yang H, Xu M, Russell JO, Pradhan-Sundd T, Liu S, Singh, Poddar M, Monga JS, Liu P, Oertel M, Ranganathan S, Singhi A, Rebouissou S, Zucman-Rossi J, Ribback S, Calvisi D, Qvartskhava N, Görg B, Häussinger D, Chen X, Monga SP. Wnt- β-catenin-GS-glutamine-mTORC1 axis in metabolic zonation and β-catenin-mutated liver tumors offers novel therapeutic opportunities. Cell Metabolism. Jan 28. pii: S1550-4131(19)30002-6. doi: 10.1016/j.cmet.2019.01.002. PMID: 30713111. Accompanying Editorial
  • Russell JO, Lu WY, Okabe H, Abrams M, Oertel M, Poddar M, Singh S, Forbes SJ, Monga SP. Hepatocyte-specific β-catenin deletion during severe liver injury provokes cholangiocytes to differentiate into hepatocytes. Hepatology. 2019 Feb;69(2):742-759. doi: 10.1002/hep.30270. Epub 2019 Jan 4. PubMed PMID: 30215850. Accompanying Editorial
  • Preziosi M, Okabe H, Poddar M, Singh S, Monga SP. Endothelial Wnts regulate β-catenin signaling in murine liver zonation and regeneration: A sequel to the Wnt-Wnt situation. Hepatol Commun. 2018 Jun 21;2(7):845-860. doi: 10.1002/hep4.1196. eCollection 2018 Jul. PubMed PMID: 30027142; PubMed Central PMCID: PMC6049069.
  • Pradhan-Sundd T, Zhou L, Vats R, Jiang A, Molina L, Singh S, Poddar M, Russell JM, Stolz DB, Oertel M, Apte U, Watkins S, Ranganathan S, Nejak-Bowen KN, Sundd P, Monga SP. Dual catenin loss in murine liver causes tight junctional deregulation and progressive intrahepatic cholestasis. Hepatology. 2017 Oct 10. doi: 10.1002/hep.29585. PubMed PMID: 29023813. Accompanying Editorial