The Role of CD36 in Stroke-Induced Inflammation and Brain Injury

Despite a well-documented role of CD36 in the pathogenesis of conditions such as atherosclerosis, inflammation and lipid metabolism, its role in cerebral ischemic injury had not been recognized at the time I initiated the study on CD36. Our report on CD36 was the first study to demonstrate the role of this receptor in inflammation and brain injury following ischemic stroke. Since CD36 is expressed in many different tissues and cell types, including peripheral monocytes/macrophages, my study also focused on the effect of CD36 expressed in the peripheral organs including bone marrow, spleen and blood. The major findings from these studies are the recognition of peripheral immunity on CNS injury, validating CD36 as a target in acute pathology, and characterizing a pharmacological agent that inhibits CD36 pathways. These studies made a major contribution toward identifying novel molecular targets that may serve as possible therapeutic strategies to attenuate acute stroke pathology.