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Abstract

Atherosclerosis is a chronic inflammatory disease characterized by gradual thickening and hardening of arteries. It is caused by the slow build up of plaque on the inner side of arterial walls that leads to the reduction of lumen diameter and restricts blood flow. This results in clinical conditions such as myocardial infarction, a leading cause of death all over the world. Epidemiological studies show that cigarette smoking is a major risk for developing this disease. Towards understanding the mechanism, we have established an animal model and found that exposure of guinea pigs to cigarette smoke (CS) causes an induction of apoptosis to aortal section. However, results showed that apoptosis is not involved in the initiation of atherosclerotic development. We also investigated the underlying mechanism of foam cell formation which is the hall mark event for the development of atherosclerosis. Since scavenger receptor CD36 plays an important role in foam cell formation, we have studied the effect of CS on CD36 expression. We observed an increased expression of CD36 in CSE treated macrophage cells. Our study revealed a new mechanism for this increased expression wherein NF-�ºB activity is involved. Currently, we are studying the effect of NF-�ºB on CS-induced foam cell formation which may provide an explanation for the rapid development of atherosclerosis in cigarette smokers.

Biography

Email: alokksil7@gmail.com