Center for Preventive Cardiology

Sergio Fazio, MD, PhD
The William and Sonja Connor
Chair of Preventive Cardiology
Professor of Medicine and Physiology & Pharmacology
Director, Center for Preventive Cardiology
Knight Cardiovascular Institute
Oregon Health and Science University
Portland, OR

Research Laboratories


The Center for Preventive Cardiology encompasses research and clinical operations focused on the study and management of lipid abnormalities and prevention of ischemia-based cardiovascular disease. Dr. Sergio Fazio is the director of the Center for Preventive Cardiology and leads the center’s research laboratory.

Current Research

The main interest of our laboratory is the understanding the pathophysiology of lipoprotein metabolism and the molecular and cellular mechanisms of atherosclerosis development. Atherosclerosis is a commonly occurring degeneration of the arterial wall, which is characterized by lipid deposition and inflammation, and represents the pathologic basis for cardiovascular diseases. Atherosclerosis-based diseases are still the number one cause of death, morbidity, hospitalizations, and days lost from work. The lipids that deposit in the arterial wall are derived from plasma lipoproteins, and accumulate as a result of hyperlipidemia, too much cholesterol in the bloodstream, or endothelial cell changes, caused by genetics, smoking, hypertension, diabetes, renal disease, and other conditions, that allow enhanced infiltration and trapping of plasma lipoproteins in to the artery wall. Our laboratory has a track record of high impact publication and federal funding on topics ranging from molecular mechanisms of hepatic uptake of postprandial lipoproteins to the role of macrophages in lipid metabolism and atherogenesis.

Among many standard methodologies used in our laboratory, we have also established the approach of bone marrow transplantation as a way to easily trace donor macrophages in an in vivo context. This has allowed us to study over the years a number of genes for their contribution to the atherosclerotic process. We have also determined the role of several proteins involved in lipid metabolism, inflammation and response to insulin signaling to the overall contribution of the cell type in atherosclerosis. Some of our work focuses on gene therapy possibilities exploiting hematopoietic stem cells and monocytes as targets of genetic engineering, resulting in the production of genes of therapeutic value in the arterial wall.

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