Myocardial infarction, the major cause of heart attack, is caused by sudden occlusion of coronary arteries. Primary cause of myocardial infarction is attributed to atherosclerosis, a disease characterized by progressive narrowing and thickening of blood vessels. It is believed that atherosclerotic plaque rupture and thrombosis cause sudden coronary artery occlusion and myocardial infarction. A number of recent papers have presented evidence that programmed cell death (apoptosis) of vascular smooth muscle cells and macrophages were found in human coronary atherosclerotic plaques. This finding has led to a paradigm that apoptosis of vascular smooth muscle cells weakens the vessel wall integrity and cause subsequent rupture. Currently, the molecular mechanisms of how death signal is received and amplified in the vascular smooth muscle cells is not well understood. It is our central hypothesis that identification and characterization of proximal and distal protein complexes from Fas pathway will provide critical information to understand apoptosis process in vascular smooth muscle cells. We will utilize novel technologies to decipher complex protein networks controlling apoptosis in the vessel wall.

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Research Project (R01)
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Pathology A Study Section (PTHA)
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Rabadan-Diehl, Cristina
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University of Connecticut
Anatomy/Cell Biology
Schools of Medicine
United States
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