Jianxin Sun, PhD

Professor of Medicine, Division of Cardiology
Associate Director, Center for Translational Medicine Director, Vascular Biology and Therapeutics Program

Jianxin Sun


1025 Walnut Street
Suite 408
Philadelphia, PA 19107

Email Jianxin Sun

215-503-5731 fax

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Jianxin Sun, PhD

Professor of Medicine, Division of Cardiology
Associate Director, Center for Translational Medicine Director, Vascular Biology and Therapeutics Program

Research & Clinical Interests

Dr. Sun’s research focuses on the molecular and cellular mechanisms involved in the regulation of endothelial dysfunction and inflammation under various pathophysiological conditions, such as atherosclerosis, restenosis, sepsis, and acute lung injury. The ultimate goal of our research is to provide clinical translation for the prevention and treatment of cardiovascular diseases.


Second Military Medical University, China, 1987
PhD Shanghai Institute of Biochemistry and Cell Biology, CAS. 1998

Most Recent Peer-Reviewed Publications

1. You B, Yan G, Chen S, Sun J. The nuclear orphan receptor Nur77 suppresses endothelial cell activation through induction of IkappaB expression. Circulation Research, 2009; 104 (6):742-9. https://www.ahajournals.org/doi/pdf/10.1161/CIRCRESAHA.108.192286

Endothelial inflammation plays a critical role in the development and progression of cardiovascular disease. We demonstrate that orphan nuclear receptor Nur77 negatively regulates the TNF-alpha- and interleukin-1beta-induced vascular EC activation by transcriptionally upregulation of IkappaBalpha expression. 

2. Li P, Zhu N, Yi B, Wang N, Chen M, You X, Zhao X, Slolomides CC, Qin Y, Sun J. MicroRNA-663 Regulates Human Vascular Smooth Muscle Cell Phenotypic Switch and Vascular Neointimal Formation.  Circulation Research, 2013; 113(10):1117-27. https://www.ahajournals.org/doi/pdf/10.1161/CIRCRESAHA.113.301306

Abnormal phenotypic switch of vascular smooth muscle cell (VSMC) is a hallmark of vascular disorders such as atherosclerosis and restenosis after angioplasty. We identify miR-663 as a novel modulator of human VSMC phenotypic switch by targeting JunB/myosin light chain 9 expression. Our results suggest that targeting miR-663 or its specific downstream targets in human VSMCs may represent an attractive approach for the treatment of proliferative vascular diseases.

3. Yang P, Wei X, Zhang J, Yi B, Zhang GX, Yin L, Yang XF, Sun J. Antithrombotic Effects of Nur77 and Nor1 Are Mediated Through Upregulating Thrombomodulin Expression in Endothelial Cells. Arterioscler Thromb Vasc Biol, 2016;36(2):361-9. https://www.ahajournals.org/doi/pdf/10.1161/ATVBAHA.115.306891 

Thrombomodulin is highly expressed on the lumenal surface of vascular endothelial cells (ECs) and possesses potent anticoagulant, antifibrinolytic, and anti-inflammatory activities in the vessel wall. We identify nuclear receptor Nur77 and Nor1 as novel regulators of thrombomodulin expression and function in vascular ECs and provide a proof-of-concept demonstration that targeted increasing expression of Nur77 and Nor1 in the vascular endothelium might represent a novel therapeutic approach for the treatment of thrombotic disorders.

4. Chen J, Zhang J, Shaik NF, Yi B, Wei X, Yang XF, Naik UP, Summer R, Yan G, Xu X, Sun J. The histone deacetylase inhibitor tubacin mitigates endothelial dysfunction by up-regulating the expression of endothelial nitric oxide synthase. J Biol Chem. 2019;294 (51):19565-19576. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6926467/pdf/zbc19565.pdf

Endothelial nitric oxide (NO) synthase (eNOS) plays a critical role in the maintenance of blood vessel homeostasis. Our findings demonstrate that HDAC6 inhibitor tubacin exhibits potent eNOS-inducing effects and suggest that this compound might be useful for the prevention or management of endothelial dysfunction-associated cardiovascular diseases.



  • Harvard Medical College