Dual effect of C-C motif chemokine receptor 5 on ischemic stroke: More harm than benefit?

Ischemic stroke involves a series of complex pathological mechanisms, of which neuroinflammation is currently the most widely recognized. C-C motif chemokine receptor 5 (CCR5) has recently been shown to be upregulated after cerebral ischemia. Notably, CCR5 is not only involved in neuroinflammation, but also in the blood-brain barrier, neural structures, and connections. Accumulating experimental studies indicate that CCR5 has a dual effect on ischemic stroke. In the acute phase after cerebral ischemia, the pro-inflammatory and disruptive effect of CCR5 on the blood-brain barrier predominates. However, in the chronic phase, the effect of CCR5 on the repair of neural structures and connections is thought to be cell-type dependent. Interestingly, clinical evidence has shown that CCR5 might be harmful rather than beneficial. CCR5-& UDelta;32 mutation or CCR5 antagonist exerts a neuroprotective effect in patients with ischemic stroke. Considering CCR5 as an attractive potential target, we introduce the current research progress of the entangled relationships between CCR5 and ischemic stroke. Clinical data are still needed to determine the efficacy of activating or inactivating CCR5 in the treatment of ischemic stroke, especially for potential phase-or cell type-dependent treatments in the future.

Automated summary

Ischemic stroke involves complex pathological mechanisms, with neuroinflammation being the most recognized. CCR5, upregulated after cerebral ischemia, plays a role in neuroinflammation as well as the blood-brain barrier, neural structures, and connections. Studies show that CCR5 has a dual effect on ischemic stroke, with pro-inflammatory effects predominating in the acute phase and potential repair effects in the chronic phase. However, clinical evidence suggests that CCR5 may be harmful. Further research is needed to determine the efficacy of targeting CCR5 in the treatment of ischemic stroke, considering potential phase or cell type-dependent approaches.