NAME: Wenjuan Liu

POSITION TITLE: Pathophysiology, Shenzhen University, Shenzhen, China

 EDUCATION/TRAINING

A.   Personal Statement

My research focus lies in myocardial hypertrophy, myocardial infarction and cardiovascular disease. I use myocardial cells and cardiac fibroblasts as a model system to monitor changes in calcium ion channel function, cytokines and inflammatory factors in cardiovascular disease. I also investigate the regulation of myocardial cells and cardiac fibroblasts ion channel function as a point to intervene in calcium signal reconstruction, and to identify new treatment strategies and drug targets for arrhythmia and other cardiovascular diseases. I have published 7 manuscripts in SCI journals such as JMCC, FRBM, AJP.

B.   Positions and Honors

Positions and Employment

0 7 /201 2 – present       Pathophysiology, Shenzhen University, Shenzhen, China

C.   Research Support

Completed Research Support

NSFC (China) (31400982)                                   01/01/2015 to 12/31/2017

Wenjuan Liu, PI                                                     ￥250,000

The mechanism of HMGB1 induce cardiomyocyte sarcoplasmic reticulum calcium leak and its role in ischemia-reperfusion injury

Youth innovation talents project of Guangdong        01/01/2015 to 12/31/2017

Wenjuan Liu, PI                                                                 ￥50,000

The role of TRIM72 in cardiac arrhythmia and its molecular mechanism

Shenzhen key project of basic research                     01/01/2015 to 12/31/2016

Wenjuan Liu, PI                                                           ￥200,000

The role of MG53 in cardiac arrhythmia and its molecular mechanism

D.   Peer-reviewed publications (*: corresponding author)

1.      Liu WJ, Chen PY, Deng JX, Lv JZ, Liu J. Resveratrol and polydatin as modulators of Ca2+ mobilization in the cardiovascular system. Ann N Y Acad Sci. 2017 Sep; 1403(1):82-91.

2.      Liu WJ, Deng JX, Wang G, Gao KP, Lin ZX, Liu SY, Wang YH, Liu J. Manipulation of KCNE2 expression modulates action potential duration and Ito and IK in rat and mouse ventricular myocytesAm J Physiol Heart Circ Physiol. 2015 Oct;309(8):H1288-302.

3.      Liu W, Deng J, Wang G, Zhang C, Luo X, Yan D, Su Q, Liu J. KCNE2 modulates cardiac L-type Ca2+ channel. J Mol Cell Cardiol 2014; 72:208-18.

4.      Jiang X*, Liu W*, Deng J, Lan L, Xue X, Zhang C, Cai G, Luo X, Liu J. Polydatin protects cardiac function against burn injury by inhibiting sarcoplasmic reticulum Ca2+ leak by reducing oxidative modification of ryanodine receptors. Free Radic Biol Med 2013; 60: 292-9.

5.      Deng J*, Liu W*, Wang Y, Dong M, Zheng M, Liu J. Polydatin modulates Ca2+ handling, excitation-contraction coupling and beta-adrenergic signaling in rat ventricular myocytes. J Mol Cell Cardiol 2012; 53(5): 646-56.

6.      Jingbo Chen*, Wenjuan Liu*, Hui Che, Jie Liu, Haiying Sun, Guirong Li. Adenosine-5'-triphosphate up-regulates proliferation in cultured human cardiac fibroblasts. Br J Pharmacol. 2012 Jun; 166(3):1140-50.

7.      Wenjuan Liu, Jianxin Deng, Jia Xu,  Haitang Wang, Meichun Yuan,  Na Liu, Yong Jiang, Jie Liu. High-mobility group box 1 (HMGB1) downregulates cardiac transient outward potassium current (Ito) through downregulation of Kv4.2 and Kv4.3 channel transcripts and proteins. J Mol Cell Cardiol. 2010 Sep; 49(3):438-48.