Advances in intervention methods and brain protection mechanisms of in situ and remote ischemic postconditioning

Ischemic postconditioning (PostC) conventionally refers to a series of brief blood vessel occlusions and reperfusions, which can induce an endogenous neuroprotective effect and reduce cerebral ischemia/reperfusion (I/R) injury. Depending on the site of adaptive ischemic intervention, PostC can be classified as in situ ischemic postconditioning (ISPostC) and remote ischemic postconditioning (RIPostC). Many studies have shown that ISPostC and RIPostC can reduce cerebral IS injury through protective mechanisms that increase cerebral blood flow after reperfusion, decrease antioxidant stress and anti-neuronal apoptosis, reduce brain edema, and regulate autophagy as well as Akt, MAPK, PKC, and KATP channel cell signaling pathways. However, few studies have compared the intervention methods, protective mechanisms, and cell signaling pathways of ISPostC and RIPostC interventions. Thus, in this article, we compare the history, common intervention methods, neuroprotective mechanisms, and cell signaling pathways of ISPostC and RIPostC.

Automated summary

Ischemic postconditioning (PostC) can reduce cerebral ischemia/reperfusion (I/R) injury through protective mechanisms, with in situ ischemic postconditioning (ISPostC) and remote ischemic postconditioning (RIPostC) acting through different cell signaling pathways. Studies have shown that both ISPostC and RIPostC can decrease brain ischemic injury through various protective mechanisms.