个人简介：

涂德珍，南京大学生物学博士，期间获得美国国立卫生研究院 (National Institutes of Health/ National Institute of Environmental Health Sciences) visiting program of NIH/NIEHs项目奖学金，赴美交流学习5年。后回国在中国科学院分子细胞卓越创新中心王红艳课题组做博士后近3年。现于安徽医科大学第一附属医院任副研究员。

研究方向：

探究脑内胆固醇代谢紊乱对神经炎症及中枢神经系统疾病（如帕金森氏症、多发性硬化症、胶质瘤）发生发展的影响。胆固醇是细胞膜的重要组分，在中枢神经系统内尤为丰富，其对神经元发生、胶质细胞增生、神经系统修复等都密切相关。那么哪些胆固醇合成代谢酶在其中发挥关键调控作用，它是如何影响胆固醇微环境，从而导致小胶质细胞、星型胶质细胞的功能改变。对胆固醇代谢在多种中枢神经系统疾病发生发展中的致病作用及分子机制的研究，试图为疾病的治疗提供新思路、新靶点。

联系方式：

邮箱：tudezhen0910101@126.com;

手机：18356466003

主持课题：

1）2022.1-2024.12：国家自然科学基金委员会，青年科学基金项目，32100701，胆固醇合成酶DHCR7调控小胶质细胞功能和帕金森氏症的研究，30万元，在研，主持。

2）2024.1-2027.12: 国家自然科学基金委员会, 面上项目, 32370933, AKT3调控巨噬细胞糖代谢及肿瘤发展的机制,  50万元, 在研, 参与。

代表性论文：

Ø 专著

1. Gao H-M, Tu D, Gao Y, Liu QY, Yang R, Liu Y, Guan T, and Hong J-S (2017) Roles of Microglia in Inflammation-Mediated Neurodegeneration: Models, Mechanisms, and Therapeutic Interventions for Parkinson’s Disease. In: Advances in Neurotoxicology (Michael Aschner and Lucio Costa, ed), Elsevier.

2. Gao H-M, Gao Y, Tu D, Liu Y, Zhou H, and Hong J-S (2018) Inflammation-Mediated Neurodegeneration: Models, Mechanisms, and Therapeutic Interventions for Neurodegenerative Diseases. In: Inflammation-from Molecular and Cellular Mechanisms to the Clinic (Jean-Marc Cavaillon & Mervyn Singer, ed), Wiley-VCH.

Ø 论文

1. Tu D, Gao Y, Yang R, Guan T, Hong J-S, Gao H-M. The pentose phosphate pathway regulates chronic neuroinflammation and dopaminergic neurodegeneration. Journal of Neuroinflammation. (2019). 16:255.

2. Tu D, Ravikanth V, Gao Y, Hong J-S, Zhou H, Gao H-M. Activation of neuronal NADPH oxidase NOX2 promotes inflammatory neurodegeneration. Free Radical Biology and Medicine. (2023). 200:47-58.

3. Zhang X^#, Tu D^#, Li S^#, Li N, Li D, Gao Y, Tian L, Liu J, Zhang X, Hong J-S, Hou L, Zhao J. A novel synthetic peptide SVHRSP attenuates dopaminergic neurodegeneration by inhibiting NADPH oxidase-mediated neuroinflammation in experimental models of Parkinson’s disease. Free Radical Biology and Medicine. (2022). 188:363-374.

4. Yang R, Gao Y, Li H, Huang W, Tu D, Yang M, Liu X, Hong J-S, Gao H-M. Posttranslational S-nitrosylation modification regulates HMGB1 secretion and promotes its pro-inflammatory and neurodegenerative effects. Cell Reports. (2022). 40(11)111330.

5. Zhao Z, Wang YB, Zhou R, Li Y, Gao Y, Tu D, Wilson B, Song S, Feng J, Hong J-S, Yakel J. A novel role of NLRP3-generated IL-1β in the acute-chronic transition of peripheral lipopolysaccharide-elicited neuroinflammation: implications for sepsis-associated neurodegeneration. Journal of Neuroinflammation. (2020). 17:64

6. Zhou R, Chen SH, Zhao Z, Tu D, Song S, Wang Y, Wang Q, Feng J, Hong JS. Complement C3 Enhances LPS-Elicited Neuroinflammation and Neurodegeneration Via the Mac1/NOX2 Pathway. Mol Neurobiol. 2023 Sep;60(9):5167-5183.

7. Yang D, Li XJ, Tu D, Li XL, Wei B. Advances in viral encephalitis: Viral transmission, host immunity, and experimental animal models. Zoological Research. (2023). 44(3):525-542.

8. Song S, Tu D, Meng C, Liu J, Wilson B, Wang Q, Shih YI, Gao HM, Hong JS. Dysfunction of the noradrenergic system drives inflammation, α-synucleinopathy, and neuronal loss in mouse colon. Frontiers in Immunology. (2023). 14:1083513.

9. Chen S-H, Han S, Hu ZF, Zhou R, Gao Y, Tu D, Gao H-M, Feng J, Wang Y, Lu RB, Hong J-S. Activation of the MAC1-Erk1/2-NOX2 pathway is required for LPS-induced sustaining reactive microgliosis, chronic neuroinflammation, and neurodegeneration. Antioxidants. (2022). 11(6)1202.

10. Gou Y, Yang D, Tian T, Zhu X, Zhang R, Ren J, Tu D, Luo Y, Miao Y, Zhao H, Wang Y, Wei B. The transcription of ZIP9 is associated with the macrophage polarization and the pathogenesis of hepatocellular carcinoma. Frontiers in Immunology. (2022). 13:725595.

11. Liu D, Zhao YJ, Qi YZ, Gao Y, Tu D, Wang YX, Gao H-M, Zhou H. Benzo(a)pyrene exposure induced neuronal loss, plaque deposition and cognitive decline in APP/PS1 mice. Journal of Neuroinflammation. (2020). 17:258

12. Gao Y, Tu D, Yang R, Chu C-H, and Hong J-S, Gao H-M. Through reducing ROS production, IL-10 suppresses caspase-1-dependent IL-1β maturation, thereby preventing chronic neuroinflammation and neurodegeneration. International Journal of Molecular Sciences. (2020). 21:465