CD36 as a Therapeutic Target for Endothelial Dysfunction in Stroke

Sunghee      Cho

doi:10.2174/138161212802002760

Abstract

Stroke pathology involves multifactorial pro-death responses, including inflammation, oxidative stress, vascular dysfunction, and activation of necrotic and apoptotic pathways. The interruption of a single specific pathway in defined stroke model systems has not been sufficient to address the multifactorial nature of stroke-induced injuries in the human population. CD36 is a class B scavenger receptor that functions in regulating normal physiological and pathological functions. CD36 pathways are activated by several distinct ligands. Convergence of these pathways results in inflammatory responses and endothelial dysfunction, which may be an underlying cause of cardio- and cerebrovascular diseases. The current review describes receptor CD36-ligand interactions relevant to endothelial function and discusses how targeting CD36 may have therapeutic utility in stroke.

Keywords: CD36, stroke, angiogenesis, inflammation, endothelial dysfunction, pro-death responses, oxidative stress, vascular dysfunction, cerebrovascular diseases, scavenger receptor.