Laboratory of Molecular Adaptations to Exercise, Graduate School of Human and Environmental Studies, Kyoto University, Yoshida-Nihonmatsu-Cho, Sakyo-Ku, Kyoto, 606-8501, Japan.
Laboratory of Sports and Exercise Medicine, Graduate School of Human and Environmental Studies, Kyoto University, Yoshida-Nihonmatsu-Cho, Sakyo-Ku, Kyoto, 606-8501, Japan.
J Physiol Sci. 2024 Oct 5;74(1):51. doi: 10.1186/s12576-024-00944-1.
Advanced glycation end products (AGEs) are risk factors for various diseases, including sarcopenia. One of the deleterious effects of AGEs is the induction of abnormal reactive oxygen species (ROS) production in skeletal muscle. However, the underlying mechanism remains poorly understood. Therefore, the aim of this study was to elucidate how AGEs induce ROS production in skeletal muscle cells. This study demonstrated that AGEs treatment promoted ROS production in myoblasts and myotubes while PKC inhibitor abolished ROS production by AGEs stimulation. Phosphorylation of p47 phox by kinases such as PKCα is required to form the Nox2 complex, which induces ROS production. In this study, AGEs treatment promoted the phosphorylation of PKCα and p47 phox in myoblasts and myotubes. Our findings suggest that AGEs promote ROS production through the phosphorylation of PKCα and p47 phox in skeletal muscle cells.
晚期糖基化终产物 (AGEs) 是多种疾病的危险因素，包括肌肉减少症。AGEs 的一种有害作用是诱导骨骼肌中异常活性氧 (ROS) 的产生。然而，其潜在机制仍知之甚少。因此，本研究旨在阐明 AGEs 如何诱导骨骼肌细胞中 ROS 的产生。本研究表明，AGEs 处理促进成肌细胞和肌管中 ROS 的产生，而 PKC 抑制剂可消除 AGEs 刺激引起的 ROS 产生。PKCα 等激酶对 p47phox 的磷酸化是形成诱导 ROS 产生的 Nox2 复合物所必需的。在本研究中，AGEs 处理促进了成肌细胞和肌管中 PKCα 和 p47phox 的磷酸化。我们的研究结果表明，AGEs 通过在骨骼肌细胞中磷酸化 PKCα 和 p47phox 来促进 ROS 的产生。
