The definition of
ischaemic stroke has been recently updated as an acute episode of neurological dysfunction caused by focal brain, spinal cord, or
retinal ischaemia in the presence of a
cerebral infarction. This "tissular" definition has highlighted the importance of pathophysiological processes underlying cerebral damage. In particular, post- ischaemic
inflammation in the brain and in the blood stream could influence crucial steps of the tissue injury/repair cascade. CC and
CXC chemokines orchestrate the inflammatory response in
atherosclerotic plaque vulnerability and
cerebral infarction. These molecules exert their activities through the binding to selective transmembrane receptors. CC and
CXC chemokines modulate crucial processes (such as inflammatory cell recruitment and activation, neuronal survival, neoangiogenesis). On the other hand,
CXC chemokines could also modulate stem cell homing, thus favouring tissue repair. Given this evidence, both CC and
CXC chemokines could represent promising therapeutic targets in primary and
secondary prevention of
ischaemic stroke. Only preliminary studies have been performed investigating treatments with selective
chemokine agonists/antagonists. In this review, we will update evidence on the role and the potential therapeutic strategies targeting CC and
CXC chemokines in the pathophysiology of
ischaemic stroke.