Jean E. Schaffer, MD
Professor of Medicine, Director, Diabetic Cardiovascular Disease Center
- Virginia Minnich Distinguished Professor of Medicine
- Director, Diabetic Cardiovascular Disease Center and Diabetes Research Center
- A.B., Biochemistry: Harvard College, Cambridge, MA (1982)
- M.D., Medicine: Harvard Medical School, Boston, MA (1986)
- Internship and Residency, Medicine: Brigham & Women's Hospital, Harvard Medical School, Boston, MA (1989)
- Fellowship Clinical, Cardiology: Beth Israel Hospital, Harvard Medical School, Boston, MA (1993)
- Post-doctoral Fellow: Whitehead Institute for Biomedical Research, MIT, Cambridge, MA (1995)
- Cardiovascular Diseases
Phi Beta Kappa
Magna cum laude, Harvard University
Cum laude, Harvard Medical School
American Heart Association Louis N. Katz Basic Science Research Prize
Heinrich Wieland Prize for Lipid Research
American Heart Association Established Investigator Award
American Society for Clinical Investigation
Washington University Special Recognition for Outstanding Faculty Mentoring
Burroughs Wellcome Clinical Scientist Award in Translational Research
Fellow, American Association for the Advancement of Science
American Association of Physicians
The worldwide epidemic of diabetes and obesity presents a formidable challenge because of the serious cardiovascular complications of these disorders. Both diabetes and obesity are known risk factors for coronary artery disease, and diabetics often have a more clinically aggressive form of the disease than their non-diabetic counterparts. Heart failure, independent of coronary atherosclerosis, is also a frequent complication that contributes significantly to increased morbidity and mortality among affected individuals. Evidence is emerging that in diabetic and obese individuals, dyslipidemia leads to fatty acid accumulation in non-adipose tissues such as the myocardium and the endothelium, which results in cellular dysfunction and cell death and contributes to organ dysfunction, a process known as lipotoxicity. Dyslipidemia also likely contributes to other end organ complications in metabolic diseases.
The goals of studies in the Schaffer lab are to characterize the fundamental cellular mechanisms of lipotoxicity, and to understand how these processes contribute to organ dysfunction in rodent models of metabolic disease. Our work involves genetic screens in cultured cells into identify key molecular players in the lipotoxic response, as well as experiments to elucidate the contributions of these genes and their products in mouse models of obesity and diabetes and in transgenic mice with lipotoxic cardiomyopathy. Our genetic screens have identified a number of non-coding RNAs (and proteins that are responsible for producing them) as key molecular players in the response to metabolic stress. These regulatory RNAs are a current focus of our work.
We are also translating our basic studies to human studies in an effort to define the correlates between altered systemic lipid metabolism and early diabetic cardiomyopathy in asymptomatic individuals with type 2 diabetes. Our long-term goal is to develop novel lipid biomarkers for diagnosing the earliest structural and functional abnormalities of the heart in diabetes and for guiding therapy that may be applied to population-based practice.