POSITION TITLE: Associate Professor; Shenzhen University School of Medicine.

EDUCATION/TRAINING

A. Personal Statement

I mainly focus in clinical and fundamental study of coronary disease, hypertension, heart failure and cardiovascular aging and have deeply investigated pathogenesis and clinical biomarker diagnosis of coronary disease for years. I involved in the establishment of Prince of Wales Hospital coronary disease clinical medicine database as one of the host participants from 2007 to 2011. There are more than 3000 cases which had been follow-up visited about 10 years. After graduation from Ph.D, I was introduced in Cardiology department in Wuhan Union Hospital as talent, and then, in the same year, was introduced to health science center of Shenzhen University by Shenzhen peacock talent programs. With cooperation of Wuhan Union hospital and The Second People's Hospital of Shenzhen, in 2011, my lab complete a clinical research of thrombus formation protein by collecting and analyzing over 300 stroke and cardiac infarction patients’ cases. In 2016 we publish the clinical research about STIM1 protein base on this database. STIM1 increasing expression could highly promote thrombogenesis with poor prognosis. In the same year, we applied relative patent (2015104472650). To date, 3 patent entered substantive examination. Currently there are 2 postdocotral fellows, 2 MD candidates and 2 technicians in my lab.

B. Positions and Honors

Positions and Employment

2006.2-2007.9 Cardiology department assistant researcher, Prince of Wales Hospital, Hong Kong, China

2011.1-2011.12 Cardiology Attending Doctor, Wuhan Union Hospital, Wuhan, China

2011.12-till now Assistant Professor, Health Science Center of Shenzhen University, Shenzhen, China

2017.7-till now Director of Ergology Group, Health Science Center of Shenzhen University, Shenzhen, China

C. Contributions to Science

1.    ROCK and relative proteins in cardiovascular disease pathology

Rho-associated kinases are found plays an important role in the pathogenesis of diverse cardiovascular diseases such as hypertension, vascular inflammation, ischaemia/reperfusion injury, left ventricular remodelling after myocardial infarction etc. Rho regulate the contractility of MLCK/MLC by controlling ROCK phosphorylation level. I published a review article about ROCK inhibitor could effectively relief cardiovascular disease syndrome in 2010. Then my group determined that patients with a high N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high ROCK activity on admission had a five-fold risk of a cardiovascular event by 2012. In the same year, we found that ROCK activity was increased in CHF and it might be associated with the mortality in CHF. ROCK activity might be a complementary biomarker to CHF risk stratification.

1)    Ming Dong, Yan BP, Yu CM. Current status of rho-associated kinases (ROCKs) in coronary atherosclerosis and vasospasm. Cardiovasc Hematol Agents Med Chem. 2009 Oct;7(4):322-30.(IF：2.3）

2)    Ming Dong, Yan BP, Liao JK, Lam YY, Yip GW, Yu CM. Rho-kinase inhibition: a novel therapeutic target for the treatment of cardiovascular diseases. Drug Discov Today. 2010 Aug;15(15-16):622-9. (IF：6.828，JCR1^st zone)

3)    Dong M, Liao JK, Yan B, Li R, Zhang M, Yu CM.A combination of increased Rho kinase activity and N-terminal pro-B-type natriuretic peptide predicts worse cardiovascular outcome in patients with acute coronary syndrome.Int J Cardiol. 2012 Aug 23. [Epub ahead of print]. (IF：7.078，JCR1^st zone)

4)    Dong M, Liao JK, Fang F, Lee AP, Yan BP, Liu M, Yu CM. Increased Rho kinase activity in congestive heart failure.European Journal of Heart Failure.2012 Sep;14(9):965-73. Epub 2012 May 15. (IF：4.896，JCR2^nd zone)

5)    Dong M, Jiang X, Liao J K, et al. Elevated rho-kinase activity as a marker indicating atherosclerosis and inflammation burden in polyvascular disease patients with concomitant coronary and peripheral arterial disease. Clinical Cardiology, 2013, 36(6):347-51.

2.    Leukocyte Telomere Length relative to cardiovascular disease

Interindividual variability in telomere length is highly heritable. Leukocyte telomere length (LTL) shortening has been

shown to be associated with the process of atherosclerosis. My lab investigated the relationship between LTL and stroke by study siblings and unrelated patients cases in 2013. Then we found that decreased LTL might be associated with ischemic stroke but unlikely to be causative.

6)    Jiang X, Dong M, Cheng J, et al. Decreased Leukocyte Telomere Length (LTL) Is Associated with Stroke but Unlikely to Be Causative[J]. Plos One, 2013, 8(7):e68254. (Joint first authors，IF: 4.9，JCR3^rd zone)

3.    Bisoprolol therapeutic mechanism in hypertension

Coronary artery disease (CAD) continues to be a leading cause of morbidity and mortality in patients with hypertension. β blockers were used as safe and effective antihypertensives with a certain degree of side effect. Bisoprolol could minimum those side effect. My lab certified that bisoprolol could relief hypertension symptom effectively by studying and follow-up visiting more than 200 patients.

7)    Lin Zepeng, Dong M, Liu Jie. Bisoprolol improved endothelial function and myocardium survival of hypertension with stable angina: a randomized double-blinded trial.[J]. European Review for Medical & Pharmacological Sciences, 2013, 17(6):794-801. (Joint first authors，IF：1.04,  JCR4^th zone)

4.    Polydatin in cardiac hypertrophy

Polydatin (PD) is a monocrystalline drug that can be isolated from a traditional Chinese herb. My lab through studying PD reveled the protective mechanism of PD in multiple cardiovascular disease such as hypertension and acute myocardial infarction. We also discovered the mechanism of trans-Polydatin protecting cardiomyocyte from ischemia-reperfusion infarction by suppressing ROCK.

8)    Ding W, Dong M, Deng J, et al. Polydatin attenuates cardiac hypertrophy through modulation of cardiac Ca2+ handling and calcineurin-NFAT signaling pathway[J]. Am J Physiol Heart Circ Physiol, 2014, 307(5):H792-802. (IF: 3.49，JCR2^nd zone)

9)    Dong M, Ding W, Liao Y, et al. Polydatin prevents hypertrophy in phenylephrine induced neonatal mouse cardiomyocytes and pressure-overload mouse models.[J]. European Journal of Pharmacology, 2014, 746:186-197. (IF: 3.0，JCR3^rd zone)

10) Dong M, trans-Polydatin protects the mouse heart against ischemia/reperfusion injury via inhibition of the renin-angiotensin system (RAS) and Rho kinase (ROCK) activity. Food Funct. 2017 Jun 21;8(6):2309-2321(IF: 3.0，JCR1^st zone)

5.    IL-37 in Atherosclerotic Disease therapy

Interleukin-37 (IL-37) is a defined member of the interleukin-1 (IL-1) family, and a pivotal anti-inflammatory cytokine in the inflammatory regulation. My lab studied more than 150 patients case with acute coronary disease demonstrated that IL-37 suppress inflammation by inhibiting ROCK activity. IL-37 expression would highly increase in acute coronary disease, therefore it could potentially be the biomarker of acute coronary disease. Furthermore, in 2015, my lab uncovered Atorvastatin could suppress the IL-37 increasing in atherosis and Smad3 might regulate IL-37.

11) Shaoyuan C, Ming D,Increased IL-37 in Atherosclerotic Disease could be Suppressed by Atorvastatin therapy. Scand J Immunol. 2015 Oct;82(4):328-36  (Joint author，IF: 2.0 , JCR4^th zone)

12) Dong Ming*, et al. Elevated Plasma IL-37 playing an important role in Acute Coronary Syndrome through suppression of ROCK activation. Oncotarget. 2017 Feb; 8(6):9686-9695 (corresponding author, IF: 5.008，JCR2^nd zone)

Store-operated Ca2+ entry (SOCE) channel protein in thrombus formation

Platelet adhesion, activation and aggregation have been proven to be essential for primary hemostasis leading to thrombus. The SOCE could promote thrombogenesis leading to ischemia stroke (IS). My group demonstrated SOCE channel proteins STIM1/Orai1 were highly expressed in exosome by testing exosomes from peripheral blood plasma. We found the high level expression of STIM/Orai1 are identical to thrombogenesis. Therefore thrombogenesis could potentially be diagnose by exosome.

13) Dong M Increased expression of STIM1/Orai1 in platelets of stroke patients predictive of poor outcomes. Eur J Neurol. 2017 Jul;24(7):912-919. (IF: 4.0，JCR2^nd zone)

D. Research Support

Completed Research Support

l National Natural Science Foundation of China（81202529）  

Dong Ming, PI                                                                                                             ￥230,000

Molecular mechanism of polydatin protection function in the mouse coronary artery ischemia/reperfusion injury

l Advanced Talents Initial Funding of Shenzhen Finance Bureau

Dong Ming, PI                                                                                                                ￥5,000,000

Molecular mechanism of polydatin protection function in the mouse coronary artery ischemia/reperfusion injury