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Wen-Xing Ding, PhD

Portrait of Wen-Xing Ding
Professor, Pharmacology, Toxicology & Therapeutics

William Warner Ambercrombie Professor

Professional Background

Dr. Wen-Xing Ding graduated from Shanghai Medical University (now Fudan University) in China in 1992 in Preventive Medicine, and then obtained a Master degree from Toxicology in 1995 at Shanghai Medical University. He then got his PhD in Molecular Toxicology in 2001 from National University of Singapore. Dr. Ding then did his Postdoc training at University of Pittsburgh in 2001 and became a research assistant professor at Department of Pathology in 2006 in University of Pittsburgh. Dr. Ding became an assistant professor in 2009 and then professor of Department of Pharmacology, Toxicology and Therapeutics in 2017 at The University of Kansas Medical Center. The Ding laboratory has been working on the role of autophagy in alcohol and drug-induced liver injury since 2009. The Ding Lab is particularly interested in how autophagy selectively removes cellular damaged/excess organelles such as mitochondria and lipid droplets in hepatocytes. The Ding lab is using cutting-edge genetic engineered mice to investigate organelle homeostasis in liver biology and pathophysiology. Dr. Ding has so far published more than 170 papers in peer-reviewed journals. His research work is currently supported by NIAAA, NIDDK and NIA. Extending his expertise to the next generation of scientists, Dr. Ding is also passionate for mentoring. So far he has mentored nine graduate students and six postdoctoral fellows, nine undergraduate summer students, two high school summer students, one medical student, and five visiting scholars from outside the United States.
In addition to research, Dr Ding has demonstrated outstanding leadership for service. Dr. Ding has been a program committee member of ASIP (American Society of Investigative Pathology) since 2014, and successfully organized symposiums in Experimental Biology Meeting for programmed non-apoptotic cell death in 2015, Autophagy and Tissue injury in 2016, mTOR and liver cancer in 2018, and Alcohol-induced tissue damage in 2019. Dr. Ding has also organized a Basic Science Symposium on autophagy and Basic Research Workshop on Non-apoptotic cell death for the AASLD (American Association for the Study of Liver Diseases) annual meeting. Dr. Ding also served as a co-chair for the Gordon Research Conference for Alcohol-induced end organ injury in 2019. Dr. Ding currently serves as an Associate Editor for Autophagy and editorial boards for several journals including Hepatology, Scientific Report and American Journal of Pathology. Dr. Ding has been serving as an ad hoc reviewer for several NIH study sections and special emphasize panels including HBPP, XNDA and AA1 and a standing member for the XNDA study section.

Education and Training
  • BM, Preventive Medicine, Shanghai Medical University, China
  • MSC, Environmental Toxicology, Shanghai Med. Univ.
  • PhD, Molecular Toxicology, National Univ. of Singapore (NUS)
Professional Affiliations
  • American Association for the Study of Liver Diseases, Fellow, 2018 - Present
  • American Association for the Study of Liver Diseases, Research Award Committee, Member, 2018 - 2021
  • American Association for the Study of Liver Diseases, -, Fellow, 2018 - Present
  • American Association for the Study of Liver Diseases, Basic Research Committee, Member, 2017 - 2020
  • American Association for the Study of Liver Diseases, Steering Committee, Member, 2016 - Present
  • Society of Toxicology , Member, 2015 - Present
  • American Society of Investigative Pathology , Member, 2013 - Present



1. My lab has long been interested in studying the role of autophagy in alcohol-induced steatosis and liver injury. We were able to demonstrate that autophagy helps to selectively remove alcohol-induced excess hepatic lipid droplets and damaged mitochondria. Mechanistically, we discovered that several transcription programs regulating hepatic autophagy and lysosomal biogenesis play critical roles in alcohol-induced liver injury. Our studies may offer novel therapeutic avenues for treating ALD by modulating autophagy.
2. My team’s recent work demonstrated that selective autophagic removal of damaged mitochondria (mitophagy) and protein adducts plays a critical role in protecting against acetaminophen-induced cell death in vitro and in vivo. We showed that PINK1-PARKIN-mediated mitophagy is critical for the removal of APAP-induced damaged mitochondria, and p62/SQSTM1 is required for the removal of APAP-adducts.
3. I have long-standing interest in studying basic mitochondrial biology including mitochondrial bioenergetics, biogenesis, dynamics and quality control. My earlier work has revealed NIX as a novel PARKIN-independent mechanism in regulating mitophagy. I also defined the ultrastructure of a novel mitochondrial morphological change: mitochondrial spheroids, as a potential alternative pathway for mitochondrial quality control. More recently, we also defined an autophagy-independent secretory pathway in regulating mitochondrial removal.
4. In contrast to the beneficial role of pharmacological activation of Nrf2 in protecting against APAP-induced liver injury, paradoxically, my team’s recent work demonstrated that over activation of cellular antioxidant stress response by persistent activation of Nrf2 contributes to liver tumorigenesis. Similarly, genetic ablation of mTORC1 in mouse liver also leads to the protection of liver injury but paradoxically promotes the early liver tumor development in autophagy-deficient mice. Our work thus supports a double-edged role of Nrf2 and mTOR in liver pathophysiology.

  • Chao, X, Wang, S, Zhao, K, Li , Y, Williams, J., A, Li , T, Chavan, H, Krishnamurthy, P, He, X., C, Li , L, Ballabio, A, Ni, H., M, Ding, W., X. 2018. Impaired TFEB-Mediated Lysosome Biogenesis and Autophagy Promote Chronic Ethanol-Induced Liver Injury and Steatosis in Mice.. Gastroenterology, 155 (3), 865-879.e12
  • Wang, S, Ni, H., M, Chao, X, Wang, H, Bridge, B, Kumer, S, Schmitt, T, De Lisle, R., C, Ballabio, A, Pacher, P, Ding, W., X. 2019. Impaired TFEB-Mediated Lysosomal Biogenesis Promotes the Development of Pancreatitis in Mice and is Associated with Human Pancreatitis. Autophagy , 20, 1-16
  • Wang, S, Ni, H., M, Chao, X, Ma, X, Bridge, B, Kumer, S, Schmitt, T, De Lisle, R., C, Ballabio, A, Pacher, P, Ding, W., X. 2019. Critical role of TFEB-mediated lysosomal Biogenesis in alcohol-induced Pancreatitis in Mice and humans. Cellular and Molecular Gastroenterology and Hepatology
  • Ni, H., M, McGill, M., R, Chao, X, Du , K, Williams, J., A, Xie, Y, Jaeschke, H, Ding, W., X. 2016. Removal of acetaminophen protein adducts by autophagy protects against acetaminophen-induced liver injury in mice.. Journal of hepatology, 65 (2), 354-62
  • Wang, H, Ni, H., M, Chao, X, Rodriguez, Y., A, Chavan, H, Wang, S., G, Krishnamurthy, P, Dobrowsky, R, Xu, D., X, Jaeschke, H, Ding, W., X. 2019. Double deletion of PINK1 and Parkin impairs hepatic mitophagy and exacerbates acetaminophen-induced liver injury in mice. Redox Biology , 20 (22), 101148
  • Ni, H., M, Woolbright, B., L, Williams, J, Copple, B, Cui, W, Luyendyk, J., P, Jaeschke, H, Ding, W., X. 2014. Nrf2 promotes the development of fibrosis and tumorigenesis in mice with defective hepatic autophagy.. Journal of hepatology, 61 (3), 617-25
  • Ni, H., M, Chao, X, Yang, H, Deng, F, Wang, S, Bai, Q, Qian, H, Cui, Y, Cui, W, Shi, Y, Zong, W., X, Wang, Z, Yang, L, Ding, W., X. 2019. Dual role of MTOR in regulating liver injury and tumorigenesis in autophagy defective mouse liver. Hepatology , 70 (6), 2142-2155
  • Jiang, X, Ding, WX, Ni, HM. 2022. VMP1 regulates hepatic lipoprotein secretion and NASH independent of autophagy.. Autophagy (26), 1-3
  • Ding, WX. 2022. Lack of Hepatic Autophagy Promotes Severity of Liver Injury but Not Steatosis. J of Hepatology (77), 1458-1459
  • Ma, X, Ding, WX. 2023. Loss of hepatic DRP1 exacerbates alcoholic hepatitis by inducing megamitochondria and mitochondrial maladaptation. Hepatology (77), 159-175.