Abstract
Atherosclerosis is a progressive disease starting with accumulation of lipids, lipoproteins, and immune cells in the arterial wall. Inflammation and the innate immune response are involved in the formation of early atherosclerotic lesion. A protein complex known as the inflammasome is stimulated to activate interleukin-1β (IL-1β) and IL-18, which are responsible for activation of inflammatory processes. Inflammasome-mediated processes are important in the process of atherosclerosis. The front of structure domains as well as IL-1, and IL-18 stands at the threshold of the adaptive immune response that accelerates full-blown atherosclerotic disease progression. This review is intended to provide new insights into the pathogenesis of atherosclerosis and indicate new potential molecular targets for therapy of this disease.
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