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.
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