Reactive oxygen species (ROS) act as signaling molecules to regulate various cell functions. Numerous studies have demonstrated ROS to be essential for the differentiation of adipocytes. Peroxiredoxins (Prxs) are a ubiquitous family of antioxidant enzymes in mammalian cells. Prx2 is present in the cytoplasm and cell membranes and demonstrates ROS scavenging activity. We focused on Prx2 involvement in regulating adipogenesis and lipid accumulation and demonstrated that Prx2 expression was upregulated during adipocyte differentiation. In addition, the silencing of Prx2 (shPrx2) inhibited adipogenesis by modulating adipogenic gene expression, and cell death was enhanced via increased ROS production in shPrx2‐3T3‐L1 cells. These results demonstrate that shPrx2 triggers adipocyte cell death and weakens adipocyte function via ROS production. Taken together, our data suggest the participation of Prx2 in adipocyte function and differentiation. Our results also imply that the downregulation of Prx2 activity could help prevent obesity. Overall, findings support the development of ROS‐based therapeutic solutions for the treatment of obesity and obesity‐related metabolic disorders.

中文翻译：

---

由于过量的 ROS 生成，过氧化物酶 2 缺乏会减少白色脂肪生成。

活性氧 (ROS) 作为信号分子来调节各种细胞功能。许多研究表明 ROS 对于脂肪细胞的分化至关重要。过氧化物酶 (Prxs) 是哺乳动物细胞中普遍存在的抗氧化酶家族。Prx2 存在于细胞质和细胞膜中，显示出 ROS 清除活性。我们专注于 Prx2 参与调节脂肪生成和脂质积累，并证明 Prx2 表达在脂肪细胞分化过程中上调。此外，Prx2 (shPrx2) 的沉默通过调节脂肪生成基因表达抑制脂肪生成，并且通过增加 shPrx2-3T3-L1 细胞中 ROS 的产生来增强细胞死亡。这些结果表明 shPrx2 通过产生 ROS 触发脂肪细胞死亡并削弱脂肪细胞功能。总之，我们的数据表明 Prx2 参与脂肪细胞功能和分化。我们的结果还意味着 Prx2 活性的下调可能有助于预防肥胖。总体而言，研究结果支持开发基于 ROS 的治疗解决方案来治疗肥胖和肥胖相关的代谢紊乱。