The inhibitor of apoptosis‐stimulating protein of p53 (iASPP) acts as a key modulator of cellular protection against oxidative stress. In the present work, we assessed the role of iASPP in the regulation of cardiomyocyte injury induced by hypoxia/reoxygenation (H/R). We found that H/R‐exposed cardiomyocytes expressed decreased levels of iASPP. The upregulation of iASPP repressed H/R‐induced injury by decreasing levels of apoptosis and reactive oxygen species production. The upregulation of iASPP increased nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2) nuclear translocation and enhanced Nrf2 activation. The overexpression of Kelch‐like ECH‐associated protein 1 reversed iASPP‐mediated promotion of Nrf2 activation. Nrf2 inhibition abrogated iASPP‐mediated cardioprotective effects in H/R‐exposed cardiomyocytes. Our work demonstrates that the upregulation of iASPP ameliorates H/R‐induced apoptosis and oxidative stress in cardiomyocytes via potentiating Nrf2 signaling via modulation of Keap1.

中文翻译：

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iASPP的上调可通过上调Nrf2信号来改善缺氧/复氧诱导的心肌细胞凋亡和氧化应激

p53的凋亡刺激蛋白抑制剂（iASPP）是细胞抵抗氧化应激的关键调节剂。在目前的工作中，我们评估了iASPP在调节由缺氧/复氧（H / R）引起的心肌细胞损伤中的作用。我们发现暴露于H / R的心肌细胞表达的iASPP水平降低。iASPP的上调通过降低细胞凋亡和活性氧产生的水平来抑制H / R诱导的损伤。iASPP的上调增加了核因子（类胡萝卜素衍生的2）样2（Nrf2）核移位，并增强了Nrf2激活。过度表达的Kelch样ECH相关蛋白1逆转了iASPP介导的Nrf2激活的促进作用。Nrf2抑制作用消除了iASPP介导的H / R暴露的心肌细胞的心脏保护作用。