A Special Interview with Prof. David Q. H. Wang
The Editorial Office of Hepatoma Research was very honored and excited to have a special interview with Prof. David Q. H. Wang, Director of Marion Bessin Liver Research Center, Albert Einstein College of Medicine, USA, on Dec 15, 2022. Prof. Amedeo Lonardo, the Editorial Board member of Hepatoma Research, asked the questions and sincerely invited Prof. Wang to share his insights on issues of common interest.
Introduction about the Interviewee
David Q. H. Wang, MD, PhD, FAASLD, AGAF, is a Professor of Medicine and Genetics in the Departments of Medicine and Genetics, and the Director of Molecular Biology and Next Generation Technology Core of Marion Bessin Liver Research Center at Albert Einstein College of Medicine in New York, USA. Dr. Wang is an elected fellow of the American Gastroenterological Association and the American Association for the Study of Liver Diseases. The long-term objectives of his research are (i) to identify gallstone (LITH) genes and investigate their genotypes and phenotypes in mice and humans, as well as to elucidate the molecular, cellular, genetic and physical-chemical mechanisms of cholesterol gallstone disease at a fundamental level; (ii) to investigate molecular, cellular, genetic and physical-chemical factors determining intestinal absorption efficiency of cholesterol and fatty acids; and (iii) to study the pathophysiology of the metabolic syndrome with a special focus on the relationship between insulin resistance and nonalcoholic fatty liver disease. Dr. Wang's research has been supported by the National Institutes of Health and research foundations for more than 25 years. He has published over 200 research papers, review articles, and editorials in numerous top peer-reviewed professional journals. In addition, he is the co-author of several leading textbooks and encyclopedia of gastroenterology, hepatology, cardiology, and lipidology. Dr. Wang has served as Chair and reviewer for the National Institutes of Health and national and international research foundations. He has also served as Guest Editor, Associate Editor, Editorial Board member, Advisory Board member, and reviewer for more than 150 national and international professional journals. Dr. Wang received the Industry Scholar Research Award from the American Digestive Health Foundation and the American Gastroenterological Association (1996-1999), the New Scholar Award from the Ellison Medical Foundation (1999-2003), the Meritorious Service Award from the Department of Veterans Affairs of the USA (2014), and the 2017 Award for Excellence in Basic/Translational Research from the European Society for Clinical Investigation.
In the interview, Prof. Wang pointed out that both the interactions of the genetic risk factors and the environmental factors contributed to the pathogenesis of Non-alcoholic fatty liver disease (NAFLD). Currently, there are no effective drugs or treatments for NAFLD, and many clinical trials are underway to try to reach it. Besides, Prof. Wang suggested using some non-invasive biomarkers. For example, microRNA 34a has been identified in humans, which is associated with NAFLD.
Details of the Interview
1). Regarding genetic risk factors (GFRs) underlying NAFLD-HCC (Hepatoma Res 2020;6:35), one might argue that these are probably underutilized in clinical practice. Do you feel that such GFR might help clinicians to identify the subset of NAFLD patients to submit to sonographic surveillance for early diagnosis of HCC? Or do you think that non-invasive assessment of hepatic fibrosis is enough?
2). Recent studies have highlighted sexual dimorphisms in health, medicine and disease patterns. We also know that both NAFLD and HCC exhibit distinct sexual dimorphic profiles. With this background in mind, I was intrigued by your group's study on sexual dimorphism in intestinal absorption and lymphatic transport of dietary lipids (J Physiol. 2021 Nov;599(22):5015-5030). Given the key role played by a leaky gut barrier in NAFLD, may I ask you how you would recommend that future studies should leverage our understanding of intestinal physiology to better understand NAFLD pathogenesis and also, do you believe that such sexual variations of intestinal physiology may also play a role in the development of HCC occurring in NAFLD and NASH individuals?
3). Type 2 diabetes (T2D) exerts a tremendous impact on several conditions of the GI tract, notably including certain cancers (Eur J Clin Invest. 2022 Nov;52(11):e13846). This seems to be a specific example of a more general phenomenon associating metabolic disorders with cancer risk (Metab Target Organ Damage 2022;2:8). Would you mind commenting on the T2D-NAFLD-primary liver cancer? Is this risk limited to HCC alone or does it also extend to intrahepatic cholangiocarcinoma? And, again, how might these notions be exploited in clinical practice?
4). Your group has identified Hepatocyte miR-34a as a key regulator in NAFLD development and progression of nonalcoholic fatty liver disease (Mol Metab. 2021 Sep;51:101244). We know that (Metab Target Organ Damage 2022; 2:12), in NAFLD pathogenesis, "factors" (i.e. components of the metabolic syndrome) and "cofactors" (notably including genetics, epigenetics, lifestyle habits and infections) interact to concur to determining disease heterogeneity (Semin Liver Dis. 2021 Nov;41(4):421-434). How do you foresee that an improved understanding of disease factors and cofactors may help develop those personalized medicine approaches in NAFLD arena that are urgently needed?
Thanks for the support from Prof. Wang and Prof. Lonardo for the special interview! It was such a pleasure to build this platform for our scholars to share and exchange their insightful views. Currently, the Special Issue "Genetic Variants in Development of Hepatocellular Carcinoma in Individuals with Alcohol-related Liver Disease" edited by Prof. Wang is calling for high-quality papers. We sincerely welcome and invite researchers in this field to submit papers to this Special Issue: https://oaemesas.com/login?JournalId=hr/?IssueId=David_special_issue.