Glutathione peroxidase 3 (Gpx3) is a pivotal selenoprotein that acts as an antioxidant. However, the role of Gpx3 in maintaining the normal metabolism of cardiomyocytes remains to be elucidated in more detail. Herein, we employed a model of Gpx3 interference in chicken embryos in vivo and Gpx3 knockdown chicken cardiomyocytes in vitro. Real-time PCR, western blotting and fluorescent staining were performed to detect reactive oxygen species (ROS), the calcium (Ca²⁺) concentration, endoplasmic reticulum (ER) stress, myocardial contraction, inflammation and heat shock proteins (HSPs). Our results revealed that Gpx3 suppression increased the level of ROS, which induced Ca²⁺ leakage in the cytoplasm by blocking the expression of Ca²⁺ channels. The imbalance of Ca²⁺ homeostasis triggered ER stress and blocked myocardial contraction. Furthermore, we found that Ca²⁺ imbalance in the cytoplasm induced severe inflammation, and HSPs might play a protective role throughout these processes. In conclusion, Gpx3 suppression induces myocardial damage through the activation of Ca²⁺-dependent ER stress.

中文翻译：

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硒蛋白 Gpx3 敲低通过鸡的 Ca2+ 泄漏诱导心肌损伤。

谷胱甘肽过氧化物酶 3 ( Gpx3 ) 是一种关键的硒蛋白，可作为抗氧化剂。然而，Gpx3在维持心肌细胞正常代谢中的作用仍有待更详细地阐明。在此，我们采用了Gpx3体内鸡胚胎干扰模型和体外Gpx3敲低鸡心肌细胞模型。进行实时 PCR、蛋白质印迹和荧光染色以检测活性氧 (ROS)、钙 (Ca ²⁺ ) 浓度、内质网 (ER) 应激、心肌收缩、炎症和热休克蛋白 (HSP)。我们的结果表明Gpx3抑制增加了 ROS 的水平，这通过阻断 Ca ²⁺通道的表达来诱导细胞质中的Ca ²⁺泄漏。Ca ²⁺稳态失衡引发内质网应激并阻止心肌收缩。此外，我们发现细胞质中的 Ca ²⁺失衡会导致严重的炎症，而 HSP 可能在这些过程中发挥保护作用。总之，Gpx3抑制通过激活 Ca ²⁺依赖性内质网应激诱导心肌损伤。