Advanced glycation end products promote ROS production via PKC/p47 phox axis in skeletal muscle cells

• Published in: The journal of physiological sciences 2024-10, Vol.74 (1), p.51, Article 51
• Main Authors: Suzuki, Shinichiro, Hayashi, Tatsuya, Egawa, Tatsuro
• Format: Article
• Language: English
• Subjects: Animals; Cell Line; Glycation End Products, Advanced - metabolism; Mice; Muscle Fibers, Skeletal - drug effects; Muscle Fibers, Skeletal - metabolism; Muscle, Skeletal - drug effects; Muscle, Skeletal - metabolism; Muscles; Myoblasts - drug effects; Myoblasts - metabolism; NADPH Oxidases - metabolism; Phosphorylation; Protein Kinase C - metabolism; Protein Kinase C-alpha - metabolism; Reactive Oxygen Species - metabolism; Short Communication; Signal Transduction - drug effects; Signal Transduction - physiology; Type 2 diabetes
• ISSN: 1880-6562; 1880-6546; 1880-6562
• 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.