Junyi Zhu, Dr. rer. nat.

• B.Sc. in Biotechnology, Hunan University, China, 2003-2007
• M.Sc. in Biomedicine, East China Normal University, China, 2007-2010
• Dr.rer.nat in Cellular & Molecular Neuroscience (equivalent to Ph.D.), Eberhard-Karls University of Tübingen, Germany, 2010-2014 
• Postdoc Fellow, Children’s National Medical Center, U.S., 2015-2017
• Postdoc Fellow, University of California Los Angeles,U.S., 2017-2019

Dr. Zhu was trained as a developmental and molecular biologist focusing on mechanisms and treatment approaches to human diseases, such as nephrotic syndrome (NS), diabetic nephropathy, congenital heart disease (CHD), and Parkinson’s disease (PD). Dr. Zhu's research at the Center for Precision Disease Modeling at the University of Maryland School of Medicine (CPDM-UMSOM) focuses on determining the roles of specific genes in the kidney, heart, and neuronal development, to understand how human patient-associated variants in these genes contribute to the pathogenesis of NS, diabetic nephropathy, CHD, PD.

Dr. Zhu received his Ph.D. training at the Hertie Institute for Clinical Brain Research, Tübingen University in Germany, working on a fly model carrying a mutant allele of the human gene Mortalin identified from German and Spanish Parkinson’s Disease patients. He generated the first Drosophila model for Mortalin-related Parkinson’s Disease and investigated molecular disease mechanisms and drug treatment approaches using this model. After completing his Ph.D. in Germany, He joined Dr. Zhe Han’s laboratory as a postdoc fellow, to continue working on Drosophila models of human diseases, especially in heart, kidney, and leukemia. In 2017, He joined Dr. Ming Guo’s laboratory at the University of California Los Angeles to study heart and kidney pathology caused by deleterious mitochondrial DNA mutations using Drosophila as a model system. In 2019, He became a faculty member as an Assistant Professor at the University of Maryland School of Medicine.

Drosophila, Heart, Kidney, Congenital heart disease, Nephrotic syndrome, Genetic kidney diseases

1. Zhu, J.Y.^#, van de Leemput, J., Han, Z.^# (2024) Distinct roles of COMPASS subunits to Drosophila heart development. Biology Open 13 (10) (^#Co-corresponding author)
2. Zhu, J.Y.^#, Duan, J., van de Leemput, J., Han, Z.^# (2024) Dysfunction of Mitochondrial Dynamics Induces Endocytosis Defect and Cell Damage in Drosophila Nephrocytes. Cells 13 (15): 1253 (^#Co-corresponding author)
3. Zhu, J.Y.^#, van de Leemput, J., Han, Z.^# (2024) Promoting mitochondrial dynamics by inhibiting the PINK1/PRKN pathway to relieve diabetic nephropathy. Disease Models & Mechanisms 17 (4) (^#Co-corresponding author)
4. Zhu, J.Y.^#, Lee, H., Huang, X., van de Leemput, J., Han, Z.^# (2023) Distinct Roles for COMPASS Core Subunits Set1, Trx, and Trr in the Epigenetic Regulation of Drosophila Heart Development. International Journal of Molecular Sciences 24 (24): 17314 (^#Co-corresponding author)
5. Zhu, J.Y., Lee, J.G., Fu, Y., van de Leemput, J., Ray, P., Han, Z. (2023) APOL1-G2 accelerates nephrocyte cell death by inhibiting the autophagy pathway. Disease Models & Mechanisms Online ahead of print
6. Fu, Y.*, Lee, J.G.*, Zhu, J.Y.*, Wen, P., van de Leemput, J., Ray, P., Han, Z. (2023) A SNARE protective pool antagonizes APOL1 renal toxicity in Drosophila nephrocytes. Cell & Bioscience 13(1): 199 (*equal contribution)
7. Zhu, J.Y.^#, Liu, C., Huang, X., van de Leemput, J., Lee, H., Han, Z.^# (2023) H3K36 di-methylation marks, mediated by Ash1 in complex with Caf1-55 and MRG15, are required during Drosophila heart development. Journal of Cardiovascular Development and Disease 10(7): 307 (^#Co-corresponding author)
8. Zhu, J.Y.^#, van de Leemput, J., Han, Z.^# (2023) The roles of histone lysine methyltransferases in heart development and disease. Journal of Cardiovascular Development and Disease 10(7): 305 (^#Co-corresponding author)
9. Zhu, J.Y., Wang, G., Huang, X., Lee, H., Lee, J.G., Yang, P., van de Leemput, J., Huang, W., Kane, M.A., Yang, P., Han, Z. (2022) SARS-CoV-2 Nsp6 causes cardiac defects through 1 MGA/MAX complex2 mediated increased glycolysis. Communications Biology 5(1): 1039
10. Wen, H.*, Zhu, J.Y.*, Fu, Y., van de Leemput, J., Han, Z. (2022) Lpt, trr and Hcf regulate histone mono- and dimethylation that are essential for Drosophila heart development. Developmental Biology 490:53-65 (*equal contribution)
11. Zhu, J.Y., Hannan S.B., Drager N., Vereshchagina, N., Krahl, A., Fu, Y., Elliott, C.J., Han, Z., Jahn, T.R., Rasse, T.M. (2021) Autophagy inhibition rescues structural and functional defects caused by the loss of mitochondrial chaperone Hsc70-5 in Drosophila. Autophagy 17(10):3160-3173
12. Zhu, J.Y.*, Huang, X.*, Fu, Y.*, Richman, A., Wang, Y., Zheng, P., Liu, Y., Han, Z. (2021) Pharmacological or genetic inhibition of hypoxia signaling attenuates oncogenic Ras-induced cancer phenotypes. Disease Models & Mechanisms 15(2) (*equal contribution)
13. Zhu, J.Y., Lee, J.G., van de Leemput, J., Lee, H., Han, Z. (2021) Functional analysis of SARS-CoV-2 proteins in Drosophila identifies Orf6-induced pathogenicity attenuated by Selinexor. Cell & Bioscience 11(1): 59
14. Zhao, F.*, Zhu, J.Y.*, Richman, A., Fu, Y., Huang, W., Chen, N., Pan, X., Yi, C., Ding, X., Wang, S., Wang, P., Nie, X., Huang, J., Yang, Y., Yu, Z., Han, Z., (2019) Mutations in NUP160 Are Implicated in Steroid-Resistant Nephrotic Syndrome. Journal of the American Society of Nephrology 30(5):840-853. (*equal contribution)
15. Zhu, J.Y.*, Fu, Y.*, Nettleton, M., Richman, A., Han, Z. (2017) High throughput in vivo functional validation of candidate congenital heart disease genes in Drosophila. eLife 6: e22617. (*equal contribution)
16. Zhu, J.Y.*, Fu, Y.*, Richman, A., Zhao, Z., Ray, P.E., Han, Z. (2017) A personalized Drosophila model of COQ2 nephropathy rescued by the wild-type human COQ2 allele and dietary Q10 supplementation. Journal of the American Society of Nephrology 28(9): 2607-2617. (*equal contribution)
17. Zhu, J.Y., Heidersbach, A., Kathiriya, I.S., Garay, B., Carver-Moore, K., Ivey, K.N., Srivastava, D., Han, Z., King, I.N. (2017) The E3 Ubiquitin Ligase Nedd4/Nedd4L is Directly Regulated by microRNA-1. Development 144(5): 866-875.
18. Zhu, J.Y.*, Fu, Y.*, Richman, A., Han, Z. (2017) Validating Candidate Congenital Heart Disease Genes in Drosophila. Bio-Protocol 7(12). (*equal contribution)
19. Fu, Y. *, Zhu, J.Y.*, Richman A., Zhang, Y., Xie, X., Das, J.R., Li, J., Ray, P.E., Han, Z. (2017) APOL1-G1 in Drosophila nephrocytes induces hypertrophy and accelerates cell death. Journal of the American Society of Nephrology 28(4): 1106-1116. (*equal contribution)
20. Fu, Y.*, Zhu, J.Y.*, Richman, A., Zhao, Z., Zhang, F., Ray, P.E., Han, Z., (2017) A Drosophila model system to assess the function of human monogenic podocyte mutations that cause nephrotic syndrome. Human Molecular Genetics 26(4): 768-780. (*equal contribution)
21. Fu, Y.*, Zhu, J.Y.*, Zhang, F.*, Richman, A, Zhao, Z., Han, Z., (2017) Comprehensive functional analysis of Rab GTPases in Drosophila. Cell & Tissue Research 368(3): 615-627. (*equal contribution)
22. Zhu, J.Y., Vereshchagina, N., Sreekumar, V., Burbulla, L.F., Costa, A.C., Daub, K.J., Woitalla D., Miguel Martins, L., Krüger, R., Rasse T.M., (2013)  Knockdown of Hsc70-5/Mortalin induces loss of synaptic mitochondria in a Drosophila Parkinson’s disease model. PLoS ONE 8(12): e83714.