Abstract
Ischemic stroke, which occurs following blockage of the blood supply to the brain, is a leading cause of death worldwide. Its main cause is atherosclerosis, a disease of the arteries characterized by the deposition of plaques of fatty material on the inner artery walls. Multiple proteins involved in the inflammation response have been identified as diagnosing biomarkers of ischemic stroke. One of these is lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), an enzyme that can hydrolyze circulating oxidized phospholipids, generating proinflammatory lysophosphatidylcholine and promoting the development of atherosclerosis. In the last two decades, a number of studies have revealed that both the concentration and the activity of Lp-PLA(2) are independent biomarkers of ischemic stroke. The US Food and Drug Administration (FDA) has approved two tests to determine Lp-PLA(2) mass and activity for predicting stroke. In this review, we summarize the biological properties of Lp-PLA(2), the detection sensitivity and limitations of Lp-PLA(2) measurement, the clinical significance and association of Lp-PLA(2) in ischemic stroke, and the prospects of therapeutic inhibition of Lp-PLA(2) as an intervention and treatment.