LAUSR

Until recently, many viewed atherosclerosis as a lipid storage disease or a bland accumulation of proliferated smooth muscle cells. How the landscape has changed! Abundant evidence now implicates intertwining pathways of inflammation as crucial to atherogenesis and its clinical consequences. Inflammatory mediators modulate the functions of vascular wall cells that provoke the disease. Multiple cell types beckoned to enter the arterial intima during atherogenesis can produce these inflammatory mediators. Actions of monocyte/macrophages and T lymphocytes implicated both adaptive and innate immunity in atherosclerosis. Indeed, many leukocyte lineages participate in chronic inflammation in the plaque. Recent evidence points to the participation of the acute inflammatory cell, the polymorphonuclear leukocytes, in plaque complication. An ongoing struggle between proinflammatory and anti-inflammatory and proresolving stimuli determine the evolution of the plaque, from its initiation through its thrombotic complications.