title: CD36 as a therapeutic target for endothelial dysfunction in stroke.
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.
authors.affiliation: Department of Neurology/ Neuroscience, Weill Cornell Medical College at Burke Medical Research Institute, 785 Mamaroneck Ave., White Plains, New York 10605, USA. suc2002@med.cornell.edu
authors.forename: Sunghee
authors.initials: S
authors.lastname: Cho
mesh_terms: D018955:CD36 Antigens / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D006801:Humans; D008024:Ligands; D009389:Neovascularization, Pathologic; D020521:Stroke / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology
chemical_list: D018955:CD36 Antigens; D008024:Ligands