Redox Signaling in Skeletal Muscle

Dear Colleagues,

Currently, cardiovascular disease (CVD) and cancer have the highest morbidity and mortality rates worldwide. They are closely related in terms of many factors, including risk factors, pathogenesis, and signaling mechanisms. Mounting evidence shows that oxidative stress has an irreplaceable role in the development and pathology of various diseases and may be critical targets for developing novel preventive and therapeutic strategies. It is caused by the overproduction of reactive oxygen species (ROS), which include both free radicals and their non-radical intermediates. The burst of ROS is associated with an imbalance between the generated ROS and the antioxidant defense systems. Overproduction of ROS has a detrimental role in the biological system by not only targeting biological molecules, such as lipids, proteins, and DNA, but also by acting as a second messenger in cellular signaling. Through targeting regulatory pathways, ROS results in cell inflammatory signal activation or programmed cell death.

Evidence supports the notion that reductions in daily physical activity are the primary causes of these diseases. Regular physical exercise stands out as a remarkable non-pharmacological strategy to control oxidative stress in numerous physiological systems. Regardless of the type of physical activity or population studied, exercise can normalize the redox imbalance. In skeletal muscle, redox signaling plays an important role in a variety of physiological processes, including muscle contraction, energy metabolism, and muscle growth and repair. During muscle contraction, ROS are produced as a result of increased oxygen consumption and electron transport in the mitochondria. These reactive species act as signaling molecules that can modulate the activity of a variety of signaling pathways involved in muscle contraction, including calcium signaling, protein phosphorylation, and gene expression. In addition, ROS also play important roles in muscle metabolism and in muscle growth and repair. They are involved in the activation of satellite cells, which are muscle stem cells that are responsible for muscle repair and regeneration and can activate signaling pathways involved in protein synthesis and muscle hypertrophy, such as the mTOR pathway.

A mechanistic understanding of oxidative stress will be vital for developing adequate guidelines in preventative medicine and therapeutic approaches to mitigate disorders and pathological conditions. Detailed knowledge of oxidative stress may play a role in CVD and cancer etiology and be relevant for clinical rehabilitation. The development of antioxidant proteins for therapeutic applications is closely connected with progress in medical biotechnology and health.

The Special Issue aims to include a collection of research articles and reviews that explore different aspects of redox signaling in skeletal muscle and its effects on CVD and cancer. Topics can cover the role of oxidative stress and antioxidant defense mechanisms in muscle physiology, the effects of exercise and nutrition on redox signaling in muscle, and the potential therapeutic applications of antioxidants in muscle-related diseases and conditions.

Dr. Tiago Fernandes
Guest Editor

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• reactive oxygen species
• skeletal muscle
• cardiac and cancer cachexia
• muscle physiology
• satellite cells
• exercise-induced ros
• redox signaling
• muscle aging
• noncoding RNAs
• cell–cell communication and blood circulation