Hongmin Ni, M.D.
Associate Professor, Pharmacology, Toxicology & Therapeutics
Technical Director The Liver Cell Isolation Core, Pharmacology, Toxicology & Therapeutics
hni@kumc.eduProfessional Background
Dr. Ni is an Associate Professor in the department of Pharmacology, Toxicology and Therapeutics at the University of Kansas Medical Center. After more than 6 years working as a surgeon, inspired by a strong desire to do basic biomedical research, she started her scientific career. Her research is focused on novel mechanisms in regulation lipid metabolism, NAFLD and obesity, necroptosis in hepatic ischemia-reperfusion injury and autophagy in alcohol- or drug-induced liver injury and tumorigenesis.
In addition to research, Dr. Ni is the technical director of the Liver Cell Isolation Core in the department. As the technical director of the Cell Isolation Core, she trained a technician and oversees the isolation of primary hepatocytes and non-parenchymal cells from human, mouse and rat. The core supports various NIH-funded projects, publications and grant applications.
Education and Training
- MD, Clinical medicine, Shanghai Jiaotong University School of Medicine, China
- MS, Clinical Science, National University of Singapore, Singapore
Professional Affiliations
- Society of Toxicology (SOT), Member, 2022 - Present
- American Association for the Study of Liver Diseases, Member, 2020 - Present
- Research Society on Alcoholism, Member, 2018 - Present
Research
Overview
1. Novel Mechanisms regulating VLDL secretion and NAFLD. Non-alcoholic fatty liver (NAFLD) is an increasing health issue around the world. We identified a novel protein vacuole membrane protein 1 (VMP1), an ER membrane protein, decreased in liver samples of mouse and human non-alcoholic steatohepatitis (NASH). We developed liver-specific VMP1 knockout mice, and found these mice had severe impaired VLDL secretion and developed NASH. We are investigating the molecular mechanisms of how VMP1 regulates in VLDL secretion and its impact on NASH. We also developed several other genetic modified animal models to perform the study. Furthermore, we are identifying other novel pathways which may regulate the development of NAFLD/NASH.
2. The role of necroptosis in hepatic ischemia-reperfusion injury.Hepatic ischemia-reperfusion (IR) injury is an important cause of liver injury that occurs in many clinical conditions including liver transplantation and liver resection surgeries. Fatty liver can exacerbate hepatic ischemia and reperfusion injury and make the shortage of donor organs worse. However, there is a huge gap in the understanding of the mechanisms by which fatty liver exacerbates hepatic ischemia and reperfusion injury, which really sparked my research interest. One of the projects is to investigate the role of necroptosis in hepatic ischemia and reperfusion injury of alcoholic fatty liver and non-alcoholic fatty liver disease. We are further characterizing the mechanisms in this animal models.
3. Autophagy in alcohol-, drug-induced liver injury and tumorigenesis. Autophagy is a major intracellular degradation pathway that is responsible for removing unnecessary or dysfunctional components. It is usually activated in response to adverse environment, such as the deprivation of nutrients or growth factors. Activation of autophagy protects against alcohol- or acetaminophen-induced liver injury. Basal autophagy is critical for maintaining hepatocyte homeostasis and is a tumor suppressor in liver tumorigenesis. We developed several genetic modification animal models and are investigating the mechanisms of autophagy in alcohol-, drug-induced liver injury and tumorigenesis.
Selected Publications
- Ma, Xiaowen, Chen, Allen, Melo, Luma, Clemente‐Sanchez, Ana, Chao, Xiaojuan, Ahmadi, Ali., Reza, Peiffer, Brandon, Sun, Zhaoli, Sesaki, Hiromi, Li, Tiangang, Wang, Xiaokun, Liu, Wanqing, Bataller, Ramon, Ni, Hong‐Min, Ding, Wen‐Xing. 2023. Loss of hepatic DRP1 exacerbates alcoholic hepatitis by inducing megamitochondria and mitochondrial maladaptation. Hepatology, 77 (1), 159-175. https://doi.org/10.1002/hep.32604
- Jiang, X., Chen, A., Ding, W.X., Ni, H.M.. 2023. VMP1 regulates hepatic lipoprotein secretion and NASH independent of autophagy. Autophagy, 19 (1), 367-369. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9809953/
- Jiang, Xiaoxiao, Fulte, Sam, Deng, Fengyan, Chen, Shiyuan, Xie, Yan, Li, Feng, Liu, Wanqing, He, Xi, Li, Linheng, Davidson, Nicholas., O, Ding, Wen-Xing , Ni, Hong-Min. 2022. Lack of VMP1 Impairs Hepatic Lipoprotein Secretion and Promotes Nonalcoholic Steatohepatitis. Journal of Hepatology, 77 (3), 619-631. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9449865/
- Chen, H., McKeen, T., Chao, X. , Deng, F., Jaeschke, H., Ding, W.X., Ni, H.M.. 2022. The role of MLKL in hepatic ischemia-reperfusion injury of alcoholic steatotic livers. International Journal of Biological Sciences, 18 (3), 1096-1106. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8771841/
- Chao, X. , Wang, S., Fulte, S., Ma, X., Ahamed , F., Cui, W., Liu, Z., Rülicke, T., Zatloukal, K., Zong, W.X., Liu , W. , Ni , H.M., Ding, W.X.. 2022. Hepatocytic p62 suppresses ductular reaction and tumorigenesis in mouse livers with mTORC1 activation and defective autophagy. Journal of Hepatology, 76 (3), 639-651. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8858859/
- Li , Y., Chao, X., Wang, S., Williams, J.., A., Ni, H.M., Ding, W.X.. 2020. Role of Mechanistic Target of Rapamycin and Autophagy in Alcohol-Induced Adipose Atrophy and Liver Injury. The American Journal of Pathology, 190 (1), 158-175. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6940593/
- 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 Roles of Mammalian Target of Rapamycin in Regulating Liver Injury and Tumorigenesis in Autophagy-Defective Mouse Liver. Hepatology (Baltimore, Md.), 70 (6), 2142-2155. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6858484/
- Ni, H., M, Chao, X, Kaseff, J, Deng, F, Wang, S, Shi, Y., H, Li , T, Ding, W., X, Jaeschke, H. 2019. Receptor-Interacting Serine/Threonine-Protein Kinase 3 (RIPK3)-Mixed Lineage Kinase Domain-Like Protein (MLKL)-Mediated Necroptosis Contributes to Ischemia-Reperfusion Injury of Steatotic Livers. The American Journal of Pathology, 189 (7), 1363-1374. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6698941/
- Chao, Xiaojuan, Wang, Shaogui, Zhao, Katrina, Li, Yuan, Williams, Jessica., A., Li, Tiangang, Chavan, Hemantkumar, Krishnamurthy, Partha, He, Xi., C., Li, Linheng, Ballabio, Andrea, Ni, Hong-Min, Ding, Wen-Xing. 2018. Impaired TFEB-Mediated Lysosome Biogenesis and Autophagy Promote Chronic Ethanol-Induced Liver Injury and Steatosis in Mice. Gastroenterology, 155 (3), 865-879.e12. https://doi.org/10.1053/j.gastro.2018.05.027
- Ni, Hong-Min, McGill, Mitchell., R., Chao, Xiaojuan, Du, Kuo, Williams, Jessica., A., Xie, Yuchao, Jaeschke, Hartmut, Ding, Wen-Xing. 2016. Removal of acetaminophen protein adducts by autophagy protects against acetaminophen-induced liver injury in mice. Journal of Hepatology, 65 (2), 354-362. https://doi.org/10.1016/j.jhep.2016.04.025