Abstract
Increasing evidence suggests that atherosclerosis may be a chronic inflammatory condition
involving a complex multifactorial process, resulting in a fibroproliferative response
to various forms of injurious stimuli to the arterial wall. The changes in the arterial
wall lead to a clinically significant event when the atherosclerotic plaque ruptures
and the thrombosis takes place. The potential interactions of cells, cytokines, and
growth regulatory molecules in the atherosclerotic lesion present numerous opportunities
for modulating lesion formation and progression. This article reviews the role interleukins
that are released from both immune and non-immune cells of vascular wall may play
on the process of atherogenesis. It is speculated that these may serve as potential
targets for therapeutic intervention.
