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DOI: 10.1160/TH10-10-0662
CC and CXC chemokines are pivotal mediators of cerebral injury in ischaemic stroke
Financial support: This work was funded by EU FP7, Grant number 201668, AtheroRemo, supported grants from the Swiss National Science Foundation (#310030–118245), De Reuter Foundation and Boninchi Foundation to Dr. F. Mach. This work was founded by the “Sir Jules Thorn Trust Reg” fund and Gustave and Simone Prévot fund to Dr. F. Montecucco.Publication History
Received:
18 October 2010
Accepted after minor revision:
30 November 2010
Publication Date:
27 November 2017 (online)
Summary
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, neoangio-genesis). 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.
* These authors equally contributed as first authors to this work.
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