Cellular and molecular studies of atherogenesis

Abstract

The lesions of atherosclerosis represent a protective, inflammatory-fibroproliferative response against the different agents which can cause the disease. With a chronic insult, the response may become excessive and thus constitute part of the disease process. The excessive response may be reversed, given sufficient opportunity for modification of the injurious factors. Approaches to modifying specific cellular interactions, growth-regulatory molecules or intracellular signaling molecules may afford opportunities for lesion prevention or regression. For further reading see [1,2].