The small ubiquitin-like modifier (SUMO) conjugation (or SUMOylation) is a post-translational protein modification mechanism activated by different stress conditions that has been recently investigated in experimental models of cerebral ischemia. The expression of SUMOylation enzymes and substrates is not restricted in the nucleus, since they are present also in the cytoplasm and on plasma membrane and are involved in several physiological and pathological conditions.

In the last decades, convincing evidence have supported the idea that the increased levels of SUMOylated proteins may induce tolerance to ischemic stress. In particular, it has been established that protein SUMOylation may confer neuroprotection during ischemic preconditioning.

Considering the increasing evidence that SUMO can modify stability and expression of ion channels and transporters and the relevance of controlling ionic homeostasis in ischemic conditions, the present review will resume the main aspects of SUMO pathways related to the key molecules involved in maintenance of ionic homeostasis during cerebral ischemia and ischemic preconditioning, with a particular focus on the on Na⁺/Ca²⁺ exchangers.

小泛素样修饰物（SUMO）偶联（或SUMOylation）是一种由不同应激条件激活的翻译后蛋白修饰机制，最近在脑缺血的实验模型中进行了研究。SUMOylation酶和底物的表达在细胞核中不受限制，因为它们也存在于细胞质和质膜中，并且涉及几种生理和病理状况。

在过去的几十年中，令人信服的证据支持了SUMO化蛋白水平升高可能诱导对缺血性应激的耐受性这一观点。特别地，已经确定蛋白质SUMOylation可以在缺血预处理中赋予神经保护作用。

考虑到越来越多的证据表明SUMO可以改变缺血状态下离子通道和转运蛋白的稳定性和表达以及控制离子稳态的相关性，本综述将继续探讨与SUMO通路中涉及维持离子稳态的关键分子有关的SUMO途径的主要方面。脑缺血和缺血预处理，尤其着眼于Na ⁺ / Ca ²⁺交换子。