背景 缺血后处理（ischemic postconditioning, IPO）是指在心肌缺血后持续再灌注前给予多次短暂的缺血/再灌注的处理方法。大量研究证实，具有信号整合重要作用的小窝蛋白（caveolin, Cav）参与了IPO的过程，对心肌缺血/再灌注损伤（ischemia/reperfusion injury, I/RI）具有保护作用。 目的 明确Cav在I/RI中发挥的作用。旨在为进一步探寻心肌I/RI药物治疗提供理论依据。 内容 Cav与IPO中多条信号转导通路有关，包括再灌注损伤补救激酶（reperfusion injury salvage kinases, RISK）途径，肿瘤坏死因子介导的生存活化因子增强（survivor actvating factor enhancement, SAFE）途径，鞘氨醇激酶（sphingosinekinase, SPK）途径，一氧化氮/环鸟苷酸/蛋白激酶G信号级联（nitric oxide/cyclic guanosine monophosphate/protein kinase G, NO/cGMP/PKG）途经，缓激肽、腺苷信号（bradykinin and adenosine′s signalling, BK/A2）途径等信号转导通路。 趋向 IPO具有重要的心肌保护作用，其保护机制十分复杂，目前尚未完全阐明，仍需进一步深入研究。
Background Ischemic postconditioning (IPO) refers to the treatment of multiple transient ischemia/reperfusion prior to continuous reperfusion following myocardial ischemia. A large number of studies have confirmed that caveolin (Cav), which plays an important role in signal integration, is involved in the process of IPO and has protective effects on myocardial ischemia/reperfusion injury(I/RI). Objective To review potential mechanisms underlying the protection of myocardia by IPO through identifying the role of Cav in I/RI. Content Cav is associated with multiple signal transduction pathways in IPO, including reperfusion injury salvage kinases(RISK) pathway, tumor necrosis factor-mediated survivor activating factor enhancement(SAFE) pathway, sphingosine kinase(SPK) pathway, nitric oxide/cyclic guanosine monophosphate/protein kinase G(NO/cGMP/PKG) pathway, bradykinin and adenosine′s signalling(BK/A2). These pathways, instead of functioning independently, may interact with each other or regulate the same targets, and as a consequence to confer protection of myocardia. Trend IPO has an important role in myocardial protection, but further research is needed to fully elucidate the complex underlying mechanisms.
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