Vascular Biology of Atherogenesis

Dr. Peter Libby directs a research laboratory that focuses on the basic mechanisms of diseases of the arteries, including atherosclerosis or hardening of the arteries. Dr. Libby and his colleagues are exploring the concept that the body's own defense mechanisms against such injury as cholesterol may eventually lead to a maladaptive reaction that leads to blood vessel disease. The research group studies various messengers produced by the body that may be involved in producing blockages in arteries. These blockages, often called arterial plaque, can trigger formation of blood clots that cause heart attacks, strokes, and gangrene of the limbs.

In addition to probing the basic mechanisms of important arterial diseases, the studies underway in these laboratories may help to understand how modern medications used to treat high cholesterol and other risk factors for heart disease may produce their benefit. Such studies may also point to new targets for developing therapies to lessen further the burden of the heart and blood vessels, stroke, and peripheral vascular disease.

Major Research Interests:

• Cell and molecular biology of vascular smooth muscle and endothelial cells
• Immune and inflammatory aspects of vascular functions and pathogenesis of blood vessel diseases
• Mechanisms of growth regulation of vascular wall cells
• Atherogenesis and mechanisms of arterial hyperplastic diseases

Dr. Peter Libby's research interest is vascular biology with special reference to atherogenesis. His group studies normal and abnormal function of smooth muscle and endothelial cells using the tools of biochemistry and cell and molecular biology. Two major themes of investigation include the control of smooth muscle cell proliferation and the immune and inflammatory functions of blood vessel wall cells. Specific projects currently underway include basic investigation of the regulation of gene expression in vascular endothelial and smooth muscle cells, and study of the cellular mechanisms of atherogenesis as well as coronary restenosis and transplant-associated arteriosclerosis.

Tanaka H, Sukhova G, Schwartz D, et al. Proliferating arterial smooth muscle cells after balloon injury express TNF-alpha but not interleukin-1 or basic fibroblast growth factor. Arteriosclerosis, Thrombosis and Vascular Biology. 16:12-18; 1996.

Galis Z, Sukhova G, Kranzhöfer R, et al. Macrophage foam cells from experimental atheroma constitutively produce matrix-degrading proteinases. Proc Nati Acad Sci (USA) 92:402-506; 1995.

Geng Y-J, Libby P. Evidence for apoptosis in advanced human atheroma. Co-localization with interleukin-1 beta-converting enzyme. Am J Path 147:251-266; 1995.

Geng Y-J, Wu Q, Muszynski M, et al. Apoptosis of vascular smooth muscle cells induced by in vitro stimulation with interferon-gamma, tumor necrosis factor-alpha, and interleukin-l-beta. Arteriosclerosis, Thrombosis and Vascular Biology. 16:19-27; 1996.