Richard & Jean Ivey Chair in Molecular Toxicology
Bachelor of Medicine Southeast University Medical College
Office: Medical Sciences Building, Room 254
Website: Feng Lab
I was originally trained as a medical doctor and had the privilege of helping patients in their journey to recovery. The work was interesting, but I had a passion for science and wanted to do something more innovative, which led me to pursue scientific research. I focused my Masters on heart failure and studied the effects of drugs in heart failure patients. As a trained cardiologist, I decided to continue research on the heart as I pursued my PhD in pharmacology in Sweden. I investigated the sympathetic regulation of cardiovascular and renal function in rats with experimental heart failure post myocardial infarction. Following my post-doctoral research on vascular function, I started my research lab at Victoria Research Laboratory, Lawson Health Research Institute before moving my lab here at Western. It’s extremely rewarding to discover molecular mechanisms of heart disease, identify new drug targets to treat heart failure, and to see your research go into clinical trials.
My overall goal is to develop a better understanding of heart function in both health and disease states. We utilize a wide range of approaches ranging from in vivo animal models to cellular and molecular biology techniques, and ultrasound imaging to study pathophysiological mechanisms of heart failure, sepsis and pathogenesis of congenital heart defects. We are currently investigating cellular and molecular mechanisms on cardiac repair after myocardial infarction, regulation of inflammatory response in sepsis, and embryonic heart development in maternal diabetes. Clinically relevant disease models and genetically altered mice are employed in our studies.
Specific Research Interests
1. Cardiac Repair Post Myocardial Infarction
The epicardium is an outside layer of epithelial cells that cover the heart. Its major function in the adult is to reduce friction between the heart and pericardial membrane during heart contractions. Notably, during embryonic heart development, the epicardium contributes to the formation of coronary arteries and growth of heart muscle. In the adult heart, the epicardium can be activated after myocardial infarction (MI). We recently demonstrated that cardiac-specific overexpression of stem cell factor (SCF) improves cardiac function and animal survival post-MI. Ongoing studies are investigating epicardial activation, manipulation of non-coding RNA expression and store-operated calcium entry (SOCE) signaling to enhance cardiac repair/remodeling post-MI.
2. Regulation of Inflammatory Response in Sepsis
Our work in this area of research is focused on signal transduction pathways by which inflammatory cytokines are produced in cardiomyocytes and how they contribute to cardiac dysfunction during sepsis. Annexin A5 (Anx5) is a phospholipid binding protein that binds to phosphatidylserine with a high affinity. We recently showed for the first time that recombinant human Anx5 treatment attenuates pro-inflammatory cytokine expression and improves cardiac function and animal survival in endotoxemia. Anx5 has the hallmarks of a treatment that may revolutionize the care of sepsis patients. Ongoing work in my lab is to further study the molecular and cellular mechanisms by which Anx5 inhibits pro-inflammatory response in sepsis using clinically relevant models of sepsis.
3. Maternal Diabetes Leading to Congenital Heart Defects
Women with pre-existing diabetes (type 1 or 2) have 3-5 times higher risk of developing congenital heart defects in their offspring. My ongoing research investigates how maternal diabetes affects fetal heart development in utero and its underlying molecular mechanisms in mice. These studies may have implications in the treatment of women with maternal diabetes to prevent adverse cardiac outcomes in the offspring. We were the first to show that endothelial nitric oxide synthase (eNOS) is pivotal to normal embryonic heart development. I am currently studying the roles of eNOS dysfunction, reactive oxygen species and microRNAs in cardiac malformation induced by maternal diabetes.
Most Rewarding Moments
As a professor, I am privileged to interact with many bright students through teaching and research. It is most rewarding to see my trainees mature and grow as health professionals, scientists and professors with very successful careers. As a researcher, it’s extremely gratifying to see your research have real-life applications. We recently patented two drugs that are related to the treatment of myocardial infarction and sepsis, one of them is currently in phase I clinical trial.
|2003-2006||Premier’s Research Excellence Award, Province of Ontario|
|2009||Dean’s Awards of Excellence for Faculty (Research), Schulich School of Medicine and Dentistry, University of Western Ontario.|
|1999-2004||Research Career Award in Health Sciences from Rx & D and CIHR, Rx & D Health Research Foundation and CIHR.|
|2005-2015||Career Investigator Award, Heart and Stroke Foundation of Ontario.|
|2017-2022||Richard and Jean Ivey Fund Chair in Molecular Toxicology, Schulich School of Medicine and Dentistry, University of Western Ontario.|
|2018-2020||Faculty Scholar, University of Western Ontario.|
See my publications on Pubmed.
Engineer A, Saiyin T, Lu X, Kucey AS, Urquhart BL, Drysdale TA, Norozi K, Feng Q. Sapropterin treatment prevents congenital heart defects induced by pregestational diabetes in mice. J Am Heart Assoc. 2018;7:e009624. Link to article.
Moazzen H, Lu X, Liu M, Feng Q. Pregestational diabetes induces fetal coronary artery malformation via reactive oxygen species signaling. Diabetes. 2015;64:1431-43. Link to article.
Arnold P, Lu X, Amirahmadi F, Brandl K, Arnold JMO, Feng Q. Recombinant human annexin A5 inhibits pro-inflammatory response and improves cardiac function and survival in mice with endotoxemia. Crit Care Med. 2014;42:e32-41. Link to article.
Xiang FL, Liu Y, Lu X, Jones DL, Feng Q. Cardiac-specific overexpression of human stem cell factor promotes epicardial activation and arteriogenesis after myocardial infarction. Circulation Heart Failure. 2014;7:831-42. Link to article.
Feng Q, Song W, Lu X, Hamilton J, Lei M, Peng T, Yee SP. Development of heart failure and congenital septal defects in mice lacking endothelial nitric oxide synthase. Circulation. 2002;106:873-879. Link to article.