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The potential mechanism and clinical application value of remote ischemic conditioning in strokeOA

中文摘要

Some studies have confirmed the neuroprotective effect of remote ischemic conditioning against stroke. Although numerous animal researches have shown that the neuroprotective effect of remote ischemic conditioning may be related to neuroinflammation, cellular immunity, apoptosis, and autophagy, the exact underlying molecular mechanisms are unclear. This review summarizes the current status of different types of remote ischemic conditioning methods in animal and clinical studies and analyzes their commonalities and differences in neuroprotective mechanisms and signaling pathways. Remote ischemic conditioning has emerged as a potential therapeutic approach for improving stroke-induced brain injury owing to its simplicity, non-invasiveness, safety, and patient tolerability. Different forms of remote ischemic conditioning exhibit distinct intervention patterns, timing, and application range. Mechanistically, remote ischemic conditioning can exert neuroprotective effects by activating the Notch1/phosphatidylinositol 3-kinase/Akt signaling pathway, improving cerebral perfusion, suppressing neuroinflammation, inhibiting cell apoptosis, activating autophagy, and promoting neural regeneration. While remote ischemic conditioning has shown potential in improving stroke outcomes, its full clinical translation has not yet been achieved.

Yajun Zhu;Xiaoguo Li;Xingwei Lei;Liuyang Tang;Daochen Wen;Bo Zeng;Xiaofeng Zhang;Zichao Huang;Zongduo Guo;

The First Affiliated Hospital of Chongqing Medical University,Chongqing,China

临床医学

Aktapoptosisautophagycerebral perfusioncerebral vascular stenosisclinical transformationhemorrhagic strokeischemic strokeneuroinflammationneuroprotectionNotch1PI3Kremote ischemic conditioningstroke

《Neural Regeneration Research》 2025 (006)

P.1613-1627 / 15

supported partly by the National Natural Science Foundation of China,No.82071332;the Chongqing Natural Science Foundation Joint Fund for Innovation and Development,No.CSTB2023NSCQ-LZX0041 (both to ZG)。

10.4103/NRR.NRR-D-23-01800

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