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付毅 研究员


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付毅 研究员



联系方式

电话: 010-82805027

邮箱: yi.fu@bjmu.edu.cn


研究方向

炎症微环境调控重大血管疾病的发病机制研究



个人简介

付毅,北京大学基础医学院生理学与病理生理学系研究员,北京大学博雅青年学者。主要研究方向为炎症微环境调控重大血管疾病的发病机制主要学术成绩包括:①针对血管微环境中诱发炎症的细胞,发现新的致炎细胞类型-血管内膜驻留巨噬细胞,还揭示血小板作为非经典免疫细胞的特异调控机制(J Clin Invest. 2025Nat Cardiovasc Res. 2023Cardiovasc Res. 2025Circ Res. 2016);②针对血管微环境中调控炎症的细胞外活性分子,不仅发现新的来源于内皮细胞的致炎分子FAM3D,扩展了对致炎分子的认识,还聚焦抗炎分子,揭示其负调控新机制(Cell Rep Med. 2023J Am Soc Nephrol. 2023Circulation 2023Cell Res. 2021)。获国家自然科学基金优秀青年基金项目资助和教育部自然科学一等奖等奖励。现任中国生理学会青年工作委员会副主任委员和基质生物学专业委员会委员以及中国免疫学会心血管免疫分会委员等。


学习经历

1999-2004 四川大学华西临床医学院 临床医学学士

2004-2009 北京大学医学部基础医学院 生理学博士


工作经历

2009-2012 澳大利亚Baker IDI Heart and Diabetes Institute 博士后 专业:血管药理学

2012-至今 北京大学医学部生理学与病理生理学系 专业:人体生理学


代表性论文

1. Fu Y, Huang Y, Yang Z, Chen Y, Zheng J, Mao C, Li Z, Liu Z, Yu B, Li T, Wang M, Xu C, Zhou Y, Zhao G, Jia Y, Guo W, Jia X, Zhang T, Li L, Liu Z, Guo S, Ma M, Zhang H, Liu B, Du J, Wang W, Tang C, Gao P, Xu Q, Wang X, Liu J, Sun J, Kong W. Cartilage oligomeric matrix protein is an endogenous β-arrestin-2-selective allosteric modulator of AT1 receptor counteracting vascular injury. Cell Res. 2021;31(7):773-790.

2. Liu Y, Liu Z, Tang H, Shen Y, Gong Z, Xie N, Zhang X, Wang W, Kong W, Zhou Y*, Fu Y*. The N6-methyladenosine (m6A)-forming enzyme METTL3 facilitates M1 macrophage polarization through the methylation of STAT1 mRNA. Am J Physiol Cell Physiol. 2019;317(4):C762-C775.

3. Ma B, Yao F, Xie N, Mao C, Liu F, Gong Z, Zhao G, Liu Z, Cai Z, Yu F, Dai R, Chen Z, Wang L, Xu Q*, Kong W*, Fu Y*. Cartilage oligomeric matrix protein is a novel notch ligand driving embryonic stem cell differentiation towards the smooth muscle lineage. J Mol Cell Cardiol. 2018;121:69-80.

4. He L#, Fu Y#, Deng J, Shen Y, Wang Y, Yu F, Xie N, Chen Z, Hong T, Peng X, Li Q, Zhou J, Han J, Wang Y, Xi J, Kong W. Deficiency of FAM3D (Family With Sequence Similarity 3, Member D), A Novel Chemokine, Attenuates Neutrophil Recruitment and Ameliorates Abdominal Aortic Aneurysm Development. Arterioscler Thromb Vasc Biol. 2018;38(7):1616-1631.

5. Fu Y, Gao C, Liang Y, Wang M, Huang Y, Ma W, Li T, Jia Y, Yu F, Zhu W, Cui Q, Li Y, Xu Q, Wang X, Kong W. Shift of Macrophage Phenotype due to Cartilage Oligomeric Matrix Protein Deficiency Drives Atherosclerotic Calcification. Circ Res. 2016;119(2):261-76.

6. Gao C#, Fu Y#, Li Y, Zhang X, Zhang L, Yu F, Xu SS, Xu Q, Zhu Y, Guan Y, Wang X, Kong W. Microsomal Prostaglandin E Synthase-1-Derived PGE2 Inhibits Vascular Smooth Muscle Cell Calcification. Arterioscler Thromb Vasc Biol. 2016;36(1):108-21.

7. Yang N, Yu F, Shao G, Fu Y*, Kong W*. The E3 ubiquitin ligase c-Cbl mediates integrin β1 ubiquitination during dilated cardiomyopathy. Biochem Biophys Res Commun. 2016;479(4):728-735.

8. Liang Y#, Fu Y#, Qi R, Wang M, Yang N, He L, Yu F, Zhang J, Yun CH, Wang X, Liu J, Kong W. Cartilage oligomeric matrix protein is a natural inhibitor of thrombin. Blood. 2015;126(7):905-14.

9. Fu Y*, Moore XL, Lee MK, Fernández-Rojo MA, Parat MO, Parton RG, Meikle PJ, Sviridov D, Chin-Dusting JP. Caveolin-1 plays a critical role in the differentiation of monocytes into macrophages. Arterioscler Thromb Vasc Biol. 2012;32(9):e117-25.

10. Fu Y, Hou Y, Fu C, Gu M, Li C, Kong W, Wang X, Shyy JY, Zhu Y. A novel mechanism of γ/δ T-lymphocyte and endothelial activation by shear stress: the role of ecto-ATP synthase β chain. Circ Res. 2011;108(4):410-7.


发表特邀综述4

1. Ma Z, Mao C, Jia Y, Fu Y*, Kong W. Extracellular matrix dynamics in vascular remodeling. Am J Physiol Cell Physiol. 2020;319(3):C481-C499.

2. Fu Y, Wang X, Kong W. Hyperhomocysteinaemia and vascular injury: advances in mechanisms and drug targets. Br J Pharmacol. 2018;175(8):1173-1189.

3. Fu Y, Kong W. Cartilage Oligomeric Matrix Protein: Matricellular and Matricrine Signaling in Cardiovascular Homeostasis and Disease. Curr Vasc Pharmacol. 2017;15(3):186-196.

4. Fu Y, Zhu Y. Ectopic ATP synthase in endothelial cells: a novel cardiovascular therapeutic target. Curr Pharm Des. 2010;16(37):4074-9.