Fuzhong Qin, MD, PhD

Associate Professor of Medicine

Education:Qin Fuzhong

M.D., Medicine, Datong University School of Medicine, P. R. China

Ph.D., Cardiovascular Physiology, State Key Laboratory of Cellular Physiology, Shanxi Medical University, P. R. China

Post-doc, Cardiovascular Medicine / Muscle Research Unit, University of Sydney School of Medicine, Australia

Post-doc, Cardiology Unit, University of Rochester School of Medicine, New York

General Field of Work:

Myocardial Biology, Cardiovascular Physiology, Cardiovascular Medicine

Affiliations other than medicine:

Evans Center for Interdisciplinary Biomedical Research
Cardiovascular Institute

Contact information:

Office/Lab:
650 Albany Street, X704
Phone: (617)-638-8051
Fax: (617)-638-8081
Email: fqin@bu.edu

Keywords:

reactive oxygen species, apoptosis, oxidative posttranslational modifications of SERCA, myocyte function, myocardial remodeling, heart failure

Summary of academic interest:

Dr. Qin is an Associate Professor in the Whitaker Cardiovascular Institute and the Cardiovascular Medicine Section. He is the Director of the Physiological Core Laboratory in the Myocardial Biology Unit / Cardiovascular Medicine Section. He is also the Manager of the Echocardiography Core in the Whitaker Cardiovascular Institute. Dr. Qin’s laboratory is interested in the role of reactive oxygen species in myocardial remodeling and dysfunction in heart failure. They are investigating the effects of catalase overexpression or pharmacological intervention on left ventricular remodeling and dysfunction in transgenic mouse models of heart failure induced by G(alpha)q overexpression as well as mouse models of human heart failure induced by chronic pressure overload or myocardial infarction. In addition, they are investigating the effects of the polyphenol S17384 or resveratrol on diastolic dysfunction in mice fed high fat and high sucrose. They assess left ventricular structure and function using conventional echocardiography, high-resolution mitral inflow and tissue Doppler echocardiography, maximal exercise test (rodent treadmill), Miller catheter and isovolumic Langendorff heart perfusion techniques. They also assess oxidative stress, myocyte apoptosis, myocyte hypertrophy and myocardial fibrosis. Another major focus in his laboratory is to study the role of oxidative posttranslational modifications of sarcoplasmic reticulum Ca2+ ATPase (SERCA2) in mediating contractile dysfunction in cardiomyocytes isolated from failing mouse hearts. They assess myocyte function and intracellular calcium transients using a video-assisted edge detection system (IonOptix) and oxidative modifications of calcium handling proteins. Their research may provide novel evidence that excessive reactive oxygen species cause oxidative posttranslational modifications of SERCA2 or other calcium handling proteins, leading to myocyte dysfunction in heart failure. Targeting specific protein oxidative posttranslational modifications may lead to novel therapeutic strategies for heart failure.

Recent Publications:

Lancel S, Qin F, Lennon SL, Zhang J, Tong X, Mazzini MJ, Kang YJ, Siwik DA, Cohen RA, Colucci WS. Oxidative posttranslational modifications mediate decreased SERCA activity and myocyte dysfunction in Galphaq-overexpressing mice. Circ Res. 2010 Jul 23;107(2):228-32. Epub 2010 May 27. PMID: 20508180 [PubMed - indexed for MEDLINE]

Qin F, Lennon-Edwards S, Lancel S, Biolo A, Siwik DA, Pimentel DR, Dorn GW, Kang YJ, Colucci WS. Cardiac-specific overexpression of catalase identifies hydrogen peroxide-dependent and -independent phases of myocardial remodeling and prevents the progression to overt heart failure in G(alpha)q-overexpressing transgenic mice. Circ Heart Fail. 2010 Mar;3(2):306-13. Epub 2009 Dec 16. PMID: 20018955 [PubMed - indexed for MEDLINE]

Biolo A, Greferath R, Siwik DA, Qin F, Valsky E, Fylaktakidou KC, Pothukanuri S, Duarte CD, Schwarz RP, Lehn JM, Nicolau C, Colucci WS. Enhanced exercise capacity in mice with severe heart failure treated with an allosteric effector of hemoglobin, myo-inositol trispyrophosphate. Proc Natl Acad Sci U S A. 2009 Feb 10;106(6):1926-9. Epub 2009 Feb 9. PMID: 19204295 [PubMed - indexed for MEDLINE]

Qin F, Biolo A, Siwik DA, Pimentel DR, Kang YJ, Colucci WS. Cardiac-Specific Overexpression of Catalase Attenuates Pathological Remodeling in Mice with Chronic Pressure Overload. Circulation. 2008;118:S352.

Qin F, Simeone M, Patel R. Inhibition of NADPH oxidase reduces myocardial oxidative stress and apoptosis and improves cardiac function in heart failure after myocardial infarction. Free Radic Biol Med. 2007 Jul 15;43(2):271-81. Epub 2007 Apr 29. PMID: 17603936 [PubMed - indexed for MEDLINE]