Wen-Xing Ding, PhD, has received the 2020 SOT Leading Edge in Basic Science Award for his recent contributions to advancing the fundamental understanding of liver toxicology and his breakthrough research on autophagy and mitophagy.
Dr. Ding received his PhD from the National University of Singapore in 2002. He then conducted his postdoctoral fellowship within the Department of Pathology at the University of Pittsburgh School of Medicine, where he quickly became a Research Associate and Research Assistant Professor. Dr. Ding joined the faculty at the University of Kansas Medical Center in 2009 as an Assistant Professor, rapidly achieving the rank of Professor in 2016. He currently serves as a tenured Professor in the Department of Pharmacology, Toxicology, and Therapeutics.
Dr. Ding’s research has been continuously funded by the National Institutes of Health since his first year as faculty; he has received 17 grants throughout his career. His work has demonstrated that autophagy, and particularly mitophagy, is an endogenous protective mechanism against alcohol- and drug-induced liver injury. His research has evinced that autophagy is induced in many cases of hepatotoxicity and other forms of liver injury and that inhibition of autophagy is detrimental in those diseases. This research enforces the idea that enhancing autophagy may be a promising approach to treating acute liver injury and chronic liver and pancreatic disease. Lysosome, an important organelle, sits at the end step for autophagy, which is often impaired in drug-induced liver injury and chronic liver disease. More recent work from Ding’s team uncovered a critical role of TFEB, a master regulator of lysosomal biogenesis, in drug- and alcohol-induced liver injury. Dr. Ding’s work highlights the potential promise to target TFEB for treating drug-induced liver injury and alcoholic and non-alcoholic fatty liver diseases. Dr. Ding’s research also involves the basic mechanisms of cell death in liver injury caused by drugs and other xenobiotics, and he has recently begun to engage with the understudied problem of alcohol-induced pancreatitis.
Extending his expertise to the next generation of scientists, Dr. Ding has mentored seven graduate students and four postdoctoral fellows, as well as seven undergraduate summer students, two high school summer students, one medical student, and five visiting scholars from outside the United States.
Dr. Ding’s publication record encompasses over 150 highly cited peer-reviewed papers, including on fundamental studies on the basic mechanisms of autophagy. Seventy-nine of these pieces have been published in the past five years. Throughout his career, he has served as a member of 15 different Editorial Boards and currently serves as an Associate Editor for Drug Metabolism and Toxicology and Autophagy. He also was the co-editor of the 2017 book Cell Death in Liver Disease. A member of six scientific societies, including SOT, Dr. Ding frequently chairs sessions at scientific meetings and has served as an invited speaker more than 100 times. He has been a member of SOT since 2015.
EDITOR’S SIDEBAR: Distinguished Toxicology Scholar Award Lecture at the SOT 59th Annual Meeting and ToxExpo
Dr. Wen-Xing Ding will deliver the Leading Edge in Basic Science Award Lecture on Wednesday, March 18, 2020, from 1:30 pm to 2:30 pm in Ballroom E of the Anaheim Convention Center. The topic of Dr. Ding’s lecture is “Autophagy: A Cellular Adaptive Mechanism and Potential Therapeutic Target for Alcohol- and Drug-Induced Tissue Damage.” The lecture abstract is as follows:
Macroautophagy (hereafter referred to as autophagy) is a major intracellular lysosomal degradation pathway that is responsible for the degradation of misfolded/damaged proteins and organelles. Autophagy is usually activated as a cellular adaptive/protective process and a quality control mechanism to maintain cellular homeostasis in response to an adverse environment, such as the deprivation of nutrients or exposure to toxic insults. Studies by the Ding laboratory revealed autophagy as a key protective mechanism against alcohol- and drug-induced liver injury by the selective removal of damaged mitochondria, protein adducts, excess lipid droplets, and drug metabolism cytochrome P450 enzymes. The Ding laboratory further demonstrated a critical role of mitochondrial dynamics in regulating mitophagy (a selective form of autophagy for removing mitochondria). Impaired/declined autophagy is closely associated with aging and contributes to liver tumorigenesis. Lysosomes sit at the end stage of autophagy via fusion with autophagosomes to form autolysosomes, where autophagic cargos are degraded. Studies of the Ding laboratory have identified that TFEB, a master transcription factor for lysosomal biogenesis, is impaired by alcohol and acetaminophen in the pancreas and liver, respectively, which promotes alcoholic hepatitis, pancreatitis, and drug-induced liver injury. Genetic and pharmacological activating autophagy and enhancing lysosomal biogenesis are promising approaches for preventing and reversing alcohol- and drug-induced tissue damage and fatty liver diseases.
